publications.yml

- abstract: Excessive fetal growth is associated with DNA methylation
    alterations in human hematopoietic stem and progenitor cells (HSPC),
    but their functional impact remains elusive. We implemented an
    integrative analysis combining single-cell epigenomics, single-cell
    transcriptomics, and in vitro analyses to functionally link DNA
    methylation changes to putative alterations of HSPC functions. We
    showed in hematopoietic stem cells (HSC) from large for gestational
    age neonates that both DNA hypermethylation and chromatin
    rearrangements target a specific network of transcription factors
    known to sustain stem cell quiescence. In parallel, we found a
    decreased expression of key genes regulating HSC differentiation
    including EGR1, KLF2, SOCS3, and JUNB. Our functional analyses
    showed that this epigenetic programming was associated with a
    decreased ability for HSCs to remain quiescent. Taken together, our
    multimodal approach using single-cell (epi)genomics showed that
    human fetal overgrowth affects hematopoietic stem cells' quiescence
    signaling via epigenetic programming.
  accessed: 2023-03-04
  author:
  - family: Pelletier
    given: Alexandre
  - family: Carrier
    given: Arnaud
  - family: Zhao
    given: Yongmei
  - family: Canouil
    given: Mickaël
  - family: Derhourhi
    given: Mehdi
  - family: Durand
    given: Emmanuelle
  - family: Berberian-Ferrato
    given: Lionel
  - family: Greally
    given: John
  - family: Hughes
    given: Francine
  - family: Froguel
    given: Philippe
  - family: Bonnefond
    given: Amélie
  - family: Delahaye
    given: Fabien
  container-title: International Journal of Molecular Sciences
  doi: 10.3390/ijms23137323
  id: pelletier_epigenetic_2022
  issn: 1422-0067
  issue: 13
  issued: 2022-06
  page: 7323
  title: Epigenetic and Transcriptomic Programming of HSC Quiescence
    Signaling in Large for Gestational Age Neonates
  type: article-journal
  url: "https://www.mdpi.com/1422-0067/23/13/7323"
  volume: 23
  journal-title: '*International Journal of Molecular Sciences*'
  date: 2022-06
  path: https://doi.org/10.3390/ijms23137323
  position: '4/12'
  first: '   '
- accessed: 2023-03-04
  author:
  - family: Mahajan
    given: Anubha
  - family: Spracklen
    given: Cassandra N.
  - family: Zhang
    given: Weihua
  - family: Ng
    given: Maggie C. Y.
  - family: Petty
    given: Lauren E.
  - family: Kitajima
    given: Hidetoshi
  - family: Yu
    given: Grace Z.
  - family: Rüeger
    given: Sina
  - family: Speidel
    given: Leo
  - family: Kim
    given: Young Jin
  - family: Horikoshi
    given: Momoko
  - family: Mercader
    given: Josep M.
  - family: Taliun
    given: Daniel
  - family: Moon
    given: Sanghoon
  - family: Kwak
    given: Soo-Heon
  - family: Robertson
    given: Neil R.
  - family: Rayner
    given: Nigel W.
  - family: Loh
    given: Marie
  - family: Kim
    given: Bong-Jo
  - family: Chiou
    given: Joshua
  - family: Miguel-Escalada
    given: Irene
  - dropping-particle: della
    family: Briotta Parolo
    given: Pietro
  - family: Lin
    given: Kuang
  - family: Bragg
    given: Fiona
  - family: Preuss
    given: Michael H.
  - family: Takeuchi
    given: Fumihiko
  - family: Nano
    given: Jana
  - family: Guo
    given: Xiuqing
  - family: Lamri
    given: Amel
  - family: Nakatochi
    given: Masahiro
  - family: Scott
    given: Robert A.
  - family: Lee
    given: Jung-Jin
  - family: Huerta-Chagoya
    given: Alicia
  - family: Graff
    given: Mariaelisa
  - family: Chai
    given: Jin-Fang
  - family: Parra
    given: Esteban J.
  - family: Yao
    given: Jie
  - family: Bielak
    given: Lawrence F.
  - family: Tabara
    given: Yasuharu
  - family: Hai
    given: Yang
  - family: Steinthorsdottir
    given: Valgerdur
  - family: Cook
    given: James P.
  - family: Kals
    given: Mart
  - family: Grarup
    given: Niels
  - family: Schmidt
    given: Ellen M.
  - family: Pan
    given: Ian
  - family: Sofer
    given: Tamar
  - family: Wuttke
    given: Matthias
  - family: Sarnowski
    given: Chloe
  - family: Gieger
    given: Christian
  - family: Nousome
    given: Darryl
  - family: Trompet
    given: Stella
  - family: Long
    given: Jirong
  - family: Sun
    given: Meng
  - family: Tong
    given: Lin
  - family: Chen
    given: Wei-Min
  - family: Ahmad
    given: Meraj
  - family: Noordam
    given: Raymond
  - family: Lim
    given: Victor J. Y.
  - family: Tam
    given: Claudia H. T.
  - family: Joo
    given: Yoonjung Yoonie
  - family: Chen
    given: Chien-Hsiun
  - family: Raffield
    given: Laura M.
  - family: Lecoeur
    given: Cécile
  - family: Prins
    given: Bram Peter
  - family: Nicolas
    given: Aude
  - family: Yanek
    given: Lisa R.
  - family: Chen
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  - family: Jensen
    given: Richard A.
  - family: Tajuddin
    given: Salman
  - family: Kabagambe
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  - family: An
    given: Ping
  - family: Xiang
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  - family: Choi
    given: Hyeok Sun
  - family: Cade
    given: Brian E.
  - family: Tan
    given: Jingyi
  - family: Flanagan
    given: Jack
  - family: Abaitua
    given: Fernando
  - family: Adair
    given: Linda S.
  - family: Adeyemo
    given: Adebowale
  - family: Aguilar-Salinas
    given: Carlos A.
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    given: Masato
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    given: Sonia S.
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    given: Alain
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  - family: Bork-Jensen
    given: Jette
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    given: Ivan
  - family: Brody
    given: Jennifer A.
  - family: Brummett
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  - family: Buchanan
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  - family: Canouil
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  - family: Chan
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    given: Miao-Li
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  - family: Chen
    given: Shyh-Huei
  - family: Chen
    given: Yuan-Tsong
  - family: Chen
    given: Zhengming
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    given: Lee-Ming
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    given: Mary
  - family: Das
    given: Swapan K.
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    given: H. Janaka
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    given: George
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    given: Latchezar
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    given: Ayo P.
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    given: Shufa
  - family: Duan
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  - family: Eckardt
    given: Kai-Uwe
  - family: Emery
    given: Leslie S.
  - family: Evans
    given: Daniel S.
  - family: Evans
    given: Michele K.
  - family: Fischer
    given: Krista
  - family: Floyd
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  - family: Ford
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  - family: Franco
    given: Oscar H.
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    given: Timothy M.
  - family: Freedman
    given: Barry I.
  - family: Fuchsberger
    given: Christian
  - family: Genter
    given: Pauline
  - family: Gerstein
    given: Hertzel C.
  - family: Giedraitis
    given: Vilmantas
  - family: González-Villalpando
    given: Clicerio
  - family: González-Villalpando
    given: Maria Elena
  - family: Goodarzi
    given: Mark O.
  - family: Gordon-Larsen
    given: Penny
  - family: Gorkin
    given: David
  - family: Gross
    given: Myron
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    given: Yu
  - family: Hackinger
    given: Sophie
  - family: Han
    given: Sohee
  - family: Hattersley
    given: Andrew T.
  - family: Herder
    given: Christian
  - family: Howard
    given: Annie-Green
  - family: Hsueh
    given: Willa
  - family: Huang
    given: Mengna
  - family: Huang
    given: Wei
  - family: Hung
    given: Yi-Jen
  - family: Hwang
    given: Mi Yeong
  - family: Hwu
    given: Chii-Min
  - family: Ichihara
    given: Sahoko
  - family: Ikram
    given: Mohammad Arfan
  - family: Ingelsson
    given: Martin
  - family: Islam
    given: Md Tariqul
  - family: Isono
    given: Masato
  - family: Jang
    given: Hye-Mi
  - family: Jasmine
    given: Farzana
  - family: Jiang
    given: Guozhi
  - family: Jonas
    given: Jost B.
  - family: Jørgensen
    given: Marit E.
  - family: Jørgensen
    given: Torben
  - family: Kamatani
    given: Yoichiro
  - family: Kandeel
    given: Fouad R.
  - family: Kasturiratne
    given: Anuradhani
  - family: Katsuya
    given: Tomohiro
  - family: Kaur
    given: Varinderpal
  - family: Kawaguchi
    given: Takahisa
  - family: Keaton
    given: Jacob M.
  - family: Kho
    given: Abel N.
  - family: Khor
    given: Chiea-Chuen
  - family: Kibriya
    given: Muhammad G.
  - family: Kim
    given: Duk-Hwan
  - family: Kohara
    given: Katsuhiko
  - family: Kriebel
    given: Jennifer
  - family: Kronenberg
    given: Florian
  - family: Kuusisto
    given: Johanna
  - family: Läll
    given: Kristi
  - family: Lange
    given: Leslie A.
  - family: Lee
    given: Myung-Shik
  - family: Lee
    given: Nanette R.
  - family: Leong
    given: Aaron
  - family: Li
    given: Liming
  - family: Li
    given: Yun
  - family: Li-Gao
    given: Ruifang
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    given: Symen
  - family: Lindgren
    given: Cecilia M.
  - family: Linneberg
    given: Allan
  - family: Liu
    given: Ching-Ti
  - family: Liu
    given: Jianjun
  - family: Locke
    given: Adam E.
  - family: Louie
    given: Tin
  - family: Luan
    given: Jian'an
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    given: Andrea O.
  - family: Luo
    given: Xi
  - family: Lv
    given: Jun
  - family: Lyssenko
    given: Valeriya
  - family: Mamakou
    given: Vasiliki
  - family: Mani
    given: K. Radha
  - family: Meitinger
    given: Thomas
  - family: Metspalu
    given: Andres
  - family: Morris
    given: Andrew D.
  - family: Nadkarni
    given: Girish N.
  - family: Nadler
    given: Jerry L.
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    given: Michael A.
  - family: Nayak
    given: Uma
  - family: Nongmaithem
    given: Suraj S.
  - family: Ntalla
    given: Ioanna
  - family: Okada
    given: Yukinori
  - family: Orozco
    given: Lorena
  - family: Patel
    given: Sanjay R.
  - family: Pereira
    given: Mark A.
  - family: Peters
    given: Annette
  - family: Pirie
    given: Fraser J.
  - family: Porneala
    given: Bianca
  - family: Prasad
    given: Gauri
  - family: Preissl
    given: Sebastian
  - family: Rasmussen-Torvik
    given: Laura J.
  - family: Reiner
    given: Alexander P.
  - family: Roden
    given: Michael
  - family: Rohde
    given: Rebecca
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    given: Kathryn
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    given: Charumathi
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    given: Maike
  - family: Sandow
    given: Kevin
  - family: Sattar
    given: Naveed
  - family: Schönherr
    given: Sebastian
  - family: Schurmann
    given: Claudia
  - family: Shahriar
    given: Mohammad
  - family: Shi
    given: Jinxiu
  - family: Shin
    given: Dong Mun
  - family: Shriner
    given: Daniel
  - family: Smith
    given: Jennifer A.
  - family: So
    given: Wing Yee
  - family: Stančáková
    given: Alena
  - family: Stilp
    given: Adrienne M.
  - family: Strauch
    given: Konstantin
  - family: Suzuki
    given: Ken
  - family: Takahashi
    given: Atsushi
  - family: Taylor
    given: Kent D.
  - family: Thorand
    given: Barbara
  - family: Thorleifsson
    given: Gudmar
  - family: Thorsteinsdottir
    given: Unnur
  - family: Tomlinson
    given: Brian
  - family: Torres
    given: Jason M.
  - family: Tsai
    given: Fuu-Jen
  - family: Tuomilehto
    given: Jaakko
  - family: Tusie-Luna
    given: Teresa
  - family: Udler
    given: Miriam S.
  - family: Valladares-Salgado
    given: Adan
  - dropping-particle: van
    family: Dam
    given: Rob M.
  - dropping-particle: van
    family: Klinken
    given: Jan B.
  - family: Varma
    given: Rohit
  - family: Vujkovic
    given: Marijana
  - family: Wacher-Rodarte
    given: Niels
  - family: Wheeler
    given: Eleanor
  - family: Whitsel
    given: Eric A.
  - family: Wickremasinghe
    given: Ananda R.
  - dropping-particle: van
    family: Dijk
    given: Ko Willems
  - family: Witte
    given: Daniel R.
  - family: Yajnik
    given: Chittaranjan S.
  - family: Yamamoto
    given: Ken
  - family: Yamauchi
    given: Toshimasa
  - family: Yengo
    given: Loïc
  - family: Yoon
    given: Kyungheon
  - family: Yu
    given: Canqing
  - family: Yuan
    given: Jian-Min
  - family: Yusuf
    given: Salim
  - family: Zhang
    given: Liang
  - family: Zheng
    given: Wei
  - literal: FinnGen
  - family: Rüeger
    given: Sina
  - dropping-particle: della
    family: Briotta Parolo
    given: Pietro
  - literal: eMERGE Consortium
  - family: Joo
    given: Yoonjung Yoonie
  - family: Hayes
    given: M. Geoffrey
  - family: Raffel
    given: Leslie J.
  - family: Igase
    given: Michiya
  - family: Ipp
    given: Eli
  - family: Redline
    given: Susan
  - family: Cho
    given: Yoon Shin
  - family: Lind
    given: Lars
  - family: Province
    given: Michael A.
  - family: Hanis
    given: Craig L.
  - family: Peyser
    given: Patricia A.
  - family: Ingelsson
    given: Erik
  - family: Zonderman
    given: Alan B.
  - family: Psaty
    given: Bruce M.
  - family: Wang
    given: Ya-Xing
  - family: Rotimi
    given: Charles N.
  - family: Becker
    given: Diane M.
  - family: Matsuda
    given: Fumihiko
  - family: Liu
    given: Yongmei
  - family: Zeggini
    given: Eleftheria
  - family: Yokota
    given: Mitsuhiro
  - family: Rich
    given: Stephen S.
  - family: Kooperberg
    given: Charles
  - family: Pankow
    given: James S.
  - family: Engert
    given: James C.
  - family: Chen
    given: Yii-Der Ida
  - family: Froguel
    given: Philippe
  - family: Wilson
    given: James G.
  - family: Sheu
    given: Wayne H. H.
  - family: Kardia
    given: Sharon L. R.
  - family: Wu
    given: Jer-Yuarn
  - family: Hayes
    given: M. Geoffrey
  - family: Ma
    given: Ronald C. W.
  - family: Wong
    given: Tien-Yin
  - family: Groop
    given: Leif
  - family: Mook-Kanamori
    given: Dennis O.
  - family: Chandak
    given: Giriraj R.
  - family: Collins
    given: Francis S.
  - family: Bharadwaj
    given: Dwaipayan
  - family: Paré
    given: Guillaume
  - family: Sale
    given: Michèle M.
  - family: Ahsan
    given: Habibul
  - family: Motala
    given: Ayesha A.
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    given: Xiao-Ou
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    given: Kyong-Soo
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    given: J. Wouter
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    given: Miguel
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    given: Roberta
  - family: Grallert
    given: Harald
  - family: Cheng
    given: Ching-Yu
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    given: Erwin P.
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    given: Abbas
  - family: Tai
    given: E-Shyong
  - family: Dupuis
    given: Josée
  - family: Kato
    given: Norihiro
  - family: Laakso
    given: Markku
  - family: Köttgen
    given: Anna
  - family: Koh
    given: Woon-Puay
  - family: Palmer
    given: Colin N. A.
  - family: Liu
    given: Simin
  - family: Abecasis
    given: Goncalo
  - family: Kooner
    given: Jaspal S.
  - family: Loos
    given: Ruth J. F.
  - family: North
    given: Kari E.
  - family: Haiman
    given: Christopher A.
  - family: Florez
    given: Jose C.
  - family: Saleheen
    given: Danish
  - family: Hansen
    given: Torben
  - family: Pedersen
    given: Oluf
  - family: Mägi
    given: Reedik
  - family: Langenberg
    given: Claudia
  - family: Wareham
    given: Nicholas J.
  - family: Maeda
    given: Shiro
  - family: Kadowaki
    given: Takashi
  - family: Lee
    given: Juyoung
  - family: Millwood
    given: Iona Y.
  - family: Walters
    given: Robin G.
  - family: Stefansson
    given: Kari
  - family: Myers
    given: Simon R.
  - family: Ferrer
    given: Jorge
  - family: Gaulton
    given: Kyle J.
  - family: Meigs
    given: James B.
  - family: Mohlke
    given: Karen L.
  - family: Gloyn
    given: Anna L.
  - family: Bowden
    given: Donald W.
  - family: Below
    given: Jennifer E.
  - family: Chambers
    given: John C.
  - family: Sim
    given: Xueling
  - family: Boehnke
    given: Michael
  - family: Rotter
    given: Jerome I.
  - family: McCarthy
    given: Mark I.
  - family: Morris
    given: Andrew P.
  container-title: Nature Genetics
  doi: 10.1038/s41588-022-01058-3
  id: mahajan_multi-ancestry_2022
  issn: 1061-4036, 1546-1718
  issue: 5
  issued: 2022-05
  page: 560-572
  title: Multi-ancestry genetic study of type 2 diabetes highlights the
    power of diverse populations for discovery and translation
  type: article-journal
  url: "https://www.nature.com/articles/s41588-022-01058-3"
  volume: 54
  journal-title: '*Nature Genetics*'
  date: 2022-05
  path: https://doi.org/10.1038/s41588-022-01058-3
  position: '90/347'
  first: '   '
- accessed: 2023-03-04
  author:
  - family: Khamis
    given: Amna
  - family: Ning
    given: Lijiao
  - family: Balkau
    given: Beverley
  - family: Bonnefond
    given: Amélie
  - family: Canouil
    given: Mickaël
  - family: Roussel
    given: Ronan
  - family: Froguel
    given: Philippe
  container-title: Diabetes & Metabolism
  doi: 10.1016/j.diabet.2022.101347
  id: khamis_epigenetic_2022
  issn: 12623636
  issue: 4
  issued: 2022-07
  page: 101347
  title: Epigenetic changes associated with hyperglycaemia exposure in
    the longitudinal D.E.S.I.R. cohort
  type: article-journal
  url: "https://linkinghub.elsevier.com/retrieve/pii/S1262363622000301"
  volume: 48
  journal-title: '*Diabetes & Metabolism*'
  date: 2022-07
  path: https://doi.org/10.1016/j.diabet.2022.101347
  position: '5/7'
  first: '   '
- abstract: "Abstract Gestational diabetes mellitus (GDM) is associated
    with increased risk of pregnancy complications and adverse perinatal
    outcomes. GDM often reoccurs and is associated with increased risk
    of subsequent diagnosis of type 2 diabetes (T2D). To improve our
    understanding of the aetiological factors and molecular processes
    driving the occurrence of GDM, including the extent to which these
    overlap with T2D pathophysiology, the GENetics of Diabetes In
    Pregnancy Consortium assembled genome-wide association studies of
    diverse ancestry in a total of 5485 women with GDM and 347 856
    without GDM. Through multi-ancestry meta-analysis, we identified
    five loci with genome-wide significant association (P < 5 × 10−8)
    with GDM, mapping to/near MTNR1B (P = 4.3 × 10−54), TCF7L2
    (P = 4.0 × 10−16), CDKAL1 (P = 1.6 × 10−14), CDKN2A-CDKN2B
    (P = 4.1 × 10−9) and HKDC1 (P = 2.9 × 10−8). Multiple lines of
    evidence pointed to the shared pathophysiology of GDM and T2D: (i)
    four of the five GDM loci (not HKDC1) have been previously reported
    at genome-wide significance for T2D; (ii) significant enrichment for
    associations with GDM at previously reported T2D loci; (iii) strong
    genetic correlation between GDM and T2D and (iv) enrichment of GDM
    associations mapping to genomic annotations in diabetes-relevant
    tissues and transcription factor binding sites. Mendelian
    randomization analyses demonstrated significant causal association
    (5% false discovery rate) of higher body mass index on increased GDM
    risk. Our results provide support for the hypothesis that GDM and
    T2D are part of the same underlying pathology but that, as
    exemplified by the HKDC1 locus, there are genetic determinants of
    GDM that are specific to glucose regulation in pregnancy."
  accessed: 2023-03-04
  author:
  - family: Pervjakova
    given: Natalia
  - family: Moen
    given: Gunn-Helen
  - family: Borges
    given: Maria-Carolina
  - family: Ferreira
    given: Teresa
  - family: Cook
    given: James P
  - family: Allard
    given: Catherine
  - family: Beaumont
    given: Robin N
  - family: Canouil
    given: Mickaël
  - family: Hatem
    given: Gad
  - family: Heiskala
    given: Anni
  - family: Joensuu
    given: Anni
  - family: Karhunen
    given: Ville
  - family: Kwak
    given: Soo Heon
  - family: Lin
    given: Frederick T J
  - family: Liu
    given: Jun
  - family: Rifas-Shiman
    given: Sheryl
  - family: Tam
    given: Claudia H
  - family: Tam
    given: Wing Hung
  - family: Thorleifsson
    given: Gudmar
  - family: Andrew
    given: Toby
  - family: Auvinen
    given: Juha
  - family: Bhowmik
    given: Bishwajit
  - family: Bonnefond
    given: Amélie
  - family: Delahaye
    given: Fabien
  - family: Demirkan
    given: Ayse
  - family: Froguel
    given: Philippe
  - family: Haller-Kikkatalo
    given: Kadri
  - family: Hardardottir
    given: Hildur
  - family: Hummel
    given: Sandra
  - family: Hussain
    given: Akhtar
  - family: Kajantie
    given: Eero
  - family: Keikkala
    given: Elina
  - family: Khamis
    given: Amna
  - family: Lahti
    given: Jari
  - family: Lekva
    given: Tove
  - family: Mustaniemi
    given: Sanna
  - family: Sommer
    given: Christine
  - family: Tagoma
    given: Aili
  - family: Tzala
    given: Evangelia
  - family: Uibo
    given: Raivo
  - family: Vääräsmäki
    given: Marja
  - family: Villa
    given: Pia M
  - family: Birkeland
    given: Kåre I
  - family: Bouchard
    given: Luigi
  - family: Duijn
    given: Cornelia M
  - family: Finer
    given: Sarah
  - family: Groop
    given: Leif
  - family: Hämäläinen
    given: Esa
  - family: Hayes
    given: Geoffrey M
  - family: Hitman
    given: Graham A
  - family: Jang
    given: Hak C
  - family: Järvelin
    given: Marjo-Riitta
  - family: Jenum
    given: Anne Karen
  - family: Laivuori
    given: Hannele
  - family: Ma
    given: Ronald C
  - family: Melander
    given: Olle
  - family: Oken
    given: Emily
  - family: Park
    given: Kyong Soo
  - family: Perron
    given: Patrice
  - family: Prasad
    given: Rashmi B
  - family: Qvigstad
    given: Elisabeth
  - family: Sebert
    given: Sylvain
  - family: Stefansson
    given: Kari
  - family: Steinthorsdottir
    given: Valgerdur
  - family: Tuomi
    given: Tiinamaija
  - family: Hivert
    given: Marie-France
  - family: Franks
    given: Paul W
  - family: McCarthy
    given: Mark I
  - family: Lindgren
    given: Cecilia M
  - family: Freathy
    given: Rachel M
  - family: Lawlor
    given: Deborah A
  - family: Morris
    given: Andrew P
  - family: Mägi
    given: Reedik
  container-title: Human Molecular Genetics
  doi: 10.1093/hmg/ddac050
  id: pervjakova_multi-ancestry_2022
  issn: 0964-6906, 1460-2083
  issue: 19
  issued: 2022-02
  page: 3377-3391
  title: Multi-ancestry genome-wide association study of gestational
    diabetes mellitus highlights genetic links with type 2 diabetes
  type: article-journal
  url: "https://academic.oup.com/hmg/article/31/19/3377/6537590"
  volume: 31
  journal-title: '*Human Molecular Genetics*'
  date: 2022-02
  path: https://doi.org/10.1093/hmg/ddac050
  position: '8/73'
  first: '   '
- abstract: OBJECTIVE Maternal glycemic dysregulation during pregnancy
    increases the risk of adverse health outcomes in her offspring, a
    risk thought to be linearly related to maternal hyperglycemia. It is
    hypothesized that changes in offspring DNA methylation (DNAm)
    underline these associations.RESEARCH DESIGN AND METHODS To address
    this hypothesis, we conducted fixed-effects meta-analyses of
    epigenome-wide association study (EWAS) results from eight birth
    cohorts investigating relationships between cord blood DNAm and
    fetal exposure to maternal glucose (Nmaximum = 3,503), insulin
    (Nmaximum = 2,062), and area under the curve of glucose (AUCgluc)
    following oral glucose tolerance tests (Nmaximum = 1,505). We
    performed lookup analyses for identified cytosine-guanine
    dinucleotides (CpGs) in independent observational cohorts to examine
    associations between DNAm and cardiometabolic traits as well as
    tissue-specific gene expression.RESULTS Greater maternal AUCgluc was
    associated with lower cord blood DNAm at neighboring CpGs cg26974062
    (β \[SE\] −0.013 \[2.1 × 10−3\], P value corrected for false
    discovery rate \[PFDR\] = 5.1 × 10−3) and cg02988288 (β \[SE\]−0.013
    \[2.3 × 10−3\], PFDR = 0.031) in TXNIP. These associations were
    attenuated in women with GDM. Lower blood DNAm at these two CpGs
    near TXNIP was associated with multiple metabolic traits later in
    life, including type 2 diabetes. TXNIP DNAm in liver biopsies was
    associated with hepatic expression of TXNIP. We observed little
    evidence of associations between either maternal glucose or insulin
    and cord blood DNAm.CONCLUSIONS Maternal hyperglycemia, as reflected
    by AUCgluc, was associated with lower cord blood DNAm at TXNIP.
    Associations between DNAm at these CpGs and metabolic traits in
    subsequent lookup analyses suggest that these may be candidate loci
    to investigate in future causal and mediation analyses.
  accessed: 2023-03-04
  author:
  - family: Tobi
    given: Elmar W.
  - family: Juvinao-Quintero
    given: Diana L.
  - family: Ronkainen
    given: Justiina
  - family: Ott
    given: Raffael
  - family: Alfano
    given: Rossella
  - family: Canouil
    given: Mickaël
  - family: Geurtsen
    given: Madelon L.
  - family: Khamis
    given: Amna
  - family: Küpers
    given: Leanne K.
  - family: Lim
    given: Ives Y.
  - family: Perron
    given: Patrice
  - family: Pesce
    given: Giancarlo
  - family: Tuhkanen
    given: Johanna
  - family: Starling
    given: Anne P.
  - family: Andrew
    given: Toby
  - family: Binder
    given: Elisabeth
  - family: Caiazzo
    given: Robert
  - family: Chan
    given: Jerry K. Y.
  - family: Gaillard
    given: Romy
  - family: Gluckman
    given: Peter D.
  - family: Keikkala
    given: Elina
  - family: Karnani
    given: Neerja
  - family: Mustaniemi
    given: Sanna
  - family: Nawrot
    given: Tim S.
  - family: Pattou
    given: François
  - family: Plusquin
    given: Michelle
  - family: Raverdy
    given: Violeta
  - family: Tan
    given: Kok Hian
  - family: Tzala
    given: Evangelia
  - family: Raikkonen
    given: Katri
  - family: Winkler
    given: Christiane
  - family: Ziegler
    given: Anette-G.
  - family: Annesi-Maesano
    given: Isabella
  - family: Bouchard
    given: Luigi
  - family: Chong
    given: Yap Seng
  - family: Dabelea
    given: Dana
  - family: Felix
    given: Janine F.
  - family: Heude
    given: Barbara
  - family: Jaddoe
    given: Vincent W. V.
  - family: Lahti
    given: Jari
  - family: Reimann
    given: Brigitte
  - family: Vääräsmäki
    given: Marja
  - family: Bonnefond
    given: Amélie
  - family: Froguel
    given: Philippe
  - family: Hummel
    given: Sandra
  - family: Kajantie
    given: Eero
  - family: Jarvelin
    given: Marjo-Riita
  - family: Steegers-Theunissen
    given: Regine P. M.
  - family: Howe
    given: Caitlin G.
  - family: Hivert
    given: Marie-France
  - family: Sebert
    given: Sylvain
  container-title: Diabetes Care
  doi: 10.2337/dc21-1701
  id: tobi_maternal_2022
  issn: 0149-5992
  issue: 3
  issued: 2022-03
  page: 614-623
  title: "Maternal Glycemic Dysregulation During Pregnancy and Neonatal
    Blood DNA Methylation: Meta-analyses of Epigenome-Wide Association
    Studies"
  title-short: Maternal Glycemic Dysregulation During Pregnancy and
    Neonatal Blood DNA Methylation
  type: article-journal
  url: "https://diabetesjournals.org/care/article/45/3/614/141057/Maternal-Glycemic-Dysregulation-During-Pregnancy"
  volume: 45
  journal-title: '*Diabetes Care*'
  date: 2022-03
  path: https://doi.org/10.2337/dc21-1701
  position: '6/51'
  first: '   '
- accessed: 2023-03-04
  author:
  - family: Wesolowska-Andersen
    given: Agata
  - family: Brorsson
    given: Caroline A.
  - family: Bizzotto
    given: Roberto
  - family: Mari
    given: Andrea
  - family: Tura
    given: Andrea
  - family: Koivula
    given: Robert
  - family: Mahajan
    given: Anubha
  - family: Vinuela
    given: Ana
  - family: Tajes
    given: Juan Fernandez
  - family: Sharma
    given: Sapna
  - family: Haid
    given: Mark
  - family: Prehn
    given: Cornelia
  - family: Artati
    given: Anna
  - family: Hong
    given: Mun-Gwan
  - family: Musholt
    given: Petra B.
  - family: Kurbasic
    given: Azra
  - family: De Masi
    given: Federico
  - family: Tsirigos
    given: Kostas
  - family: Pedersen
    given: Helle Krogh
  - family: Gudmundsdottir
    given: Valborg
  - family: Thomas
    given: Cecilia Engel
  - family: Banasik
    given: Karina
  - family: Jennison
    given: Chrisopher
  - family: Jones
    given: Angus
  - family: Kennedy
    given: Gwen
  - family: Bell
    given: Jimmy
  - family: Thomas
    given: Louise
  - family: Frost
    given: Gary
  - family: Thomsen
    given: Henrik
  - family: Allin
    given: Kristine
  - family: Hansen
    given: Tue Haldor
  - family: Vestergaard
    given: Henrik
  - family: Hansen
    given: Torben
  - family: Rutters
    given: Femke
  - family: Elders
    given: Petra
  - family: t'Hart
    given: Leen
  - family: Bonnefond
    given: Amelie
  - family: Canouil
    given: Mickaël
  - family: Brage
    given: Soren
  - family: Kokkola
    given: Tarja
  - family: Heggie
    given: Alison
  - family: McEvoy
    given: Donna
  - family: Hattersley
    given: Andrew
  - family: McDonald
    given: Timothy
  - family: Teare
    given: Harriet
  - family: Ridderstrale
    given: Martin
  - family: Walker
    given: Mark
  - family: Forgie
    given: Ian
  - family: Giordano
    given: Giuseppe N.
  - family: Froguel
    given: Philippe
  - family: Pavo
    given: Imre
  - family: Ruetten
    given: Hartmut
  - family: Pedersen
    given: Oluf
  - family: Dermitzakis
    given: Emmanouil
  - family: Franks
    given: Paul W.
  - family: Schwenk
    given: Jochen M.
  - family: Adamski
    given: Jerzy
  - family: Pearson
    given: Ewan
  - family: McCarthy
    given: Mark I.
  - family: Brunak
    given: Søren
  container-title: Cell Reports Medicine
  doi: 10.1016/j.xcrm.2021.100477
  id: wesolowska-andersen_four_2022
  issn: 26663791
  issue: 1
  issued: 2022-01
  page: 100477
  title: "Four groups of type 2 diabetes contribute to the etiological
    and clinical heterogeneity in newly diagnosed individuals: An IMI
    DIRECT study"
  title-short: Four groups of type 2 diabetes contribute to the
    etiological and clinical heterogeneity in newly diagnosed
    individuals
  type: article-journal
  url: "https://linkinghub.elsevier.com/retrieve/pii/S2666379121003499"
  volume: 3
  journal-title: '*Cell Reports Medicine*'
  date: 2022-01
  path: https://doi.org/10.1016/j.xcrm.2021.100477
  position: '38/60'
  first: '   '
- abstract: Recent advances in genetic analysis have significantly
    helped in progressively attenuating the heritability gap of obesity
    and have brought into focus monogenic variants that disrupt the
    melanocortin signaling. In a previous study, next-generation
    sequencing revealed a monogenic etiology in ∼50% of the children
    with severe obesity from a consanguineous population in Pakistan.
    Here we assess rare variants in obesity-causing genes in young
    adults with severe obesity from the same region. Genomic DNA from
    126 randomly selected young adult obese subjects (BMI 37.2 ± 0.3
    kg/m2; age 18.4 ± 0.3 years) was screened by conventional or
    augmented whole-exome analysis for point mutations and copy number
    variants (CNVs). Leptin, insulin, and cortisol levels were measured
    by ELISA. We identified 13 subjects carrying 13 different pathogenic
    or likely pathogenic variants in LEPR, PCSK1, MC4R, NTRK2, POMC,
    SH2B1, and SIM1. We also identified for the first time in the human,
    two homozygous stop-gain mutations in ASNSD1 and IFI16 genes.
    Inactivation of these genes in mouse models has been shown to result
    in obesity. Additionally, we describe nine homozygous mutations
    (seven missense, one stop-gain, and one stop-loss) and four
    copy-loss CNVs in genes or genomic regions previously linked to
    obesity-associated traits by genome-wide association studies.
    Unexpectedly, in contrast to obese children, pathogenic mutations in
    LEP and LEPR were either absent or rare in this cohort of young
    adults. High morbidity and mortality risks and social disadvantage
    of children with LEP or LEPR deficiency may in part explain this
    difference between the two cohorts.
  accessed: 2023-03-04
  author:
  - family: Saeed
    given: Sadia
  - family: Janjua
    given: Qasim M.
  - family: Haseeb
    given: Attiya
  - family: Khanam
    given: Roohia
  - family: Durand
    given: Emmanuelle
  - family: Vaillant
    given: Emmanuel
  - family: Ning
    given: Lijiao
  - family: Badreddine
    given: Alaa
  - family: Berberian
    given: Lionel
  - family: Boissel
    given: Mathilde
  - family: Amanzougarene
    given: Souhila
  - family: Canouil
    given: Mickaël
  - family: Derhourhi
    given: Mehdi
  - family: Bonnefond
    given: Amélie
  - family: Arslan
    given: Muhammad
  - family: Froguel
    given: Philippe
  container-title: Diabetes
  doi: 10.2337/db21-0373
  id: saeed_rare_2022
  issn: 0012-1797
  issue: 4
  issued: 2022-04
  page: 694-705
  title: Rare Variant Analysis of Obesity-Associated Genes in Young
    Adults With Severe Obesity From a Consanguineous Population of
    Pakistan
  type: article-journal
  url: "https://diabetesjournals.org/diabetes/article/71/4/694/140942/Rare-Variant-Analysis-of-Obesity-Associated-Genes"
  volume: 71
  journal-title: '*Diabetes*'
  date: 2022-04
  path: https://doi.org/10.2337/db21-0373
  position: '12/16'
  first: '   '
- abstract: "AbstractThe hepatokine follistatin is elevated in patients
    with type 2 diabetes (T2D) and promotes hyperglycemia in mice. Here
    we explore the relationship of plasma follistatin levels with
    incident T2D and mechanisms involved. Adjusted hazard ratio (HR) per
    standard deviation (SD) increase in follistatin levels for T2D is
    1.24 (CI: 1.04--1.47, p  \\<\\< 0.05) during 19-year follow-up ( n
     = 4060, Sweden); and 1.31 (CI: 1.09--1.58, p  \\<\\< 0.01) during
    4-year follow-up ( n  = 883, Finland). High circulating follistatin
    associates with adipose tissue insulin resistance and non-alcoholic
    fatty liver disease ( n  = 210, Germany). In human adipocytes,
    follistatin dose-dependently increases free fatty acid release. In
    genome-wide association study (GWAS), variation in the glucokinase
    regulatory protein gene ( GCKR ) associates with plasma follistatin
    levels ( n  = 4239, Sweden; n  = 885, UK, Italy and Sweden) and GCKR
    regulates follistatin secretion in hepatocytes in vitro. Our
    findings suggest that GCKR regulates follistatin secretion and that
    elevated circulating follistatin associates with an increased risk
    of T2D by inducing adipose tissue insulin resistance."
  accessed: 2023-03-04
  author:
  - family: Wu
    given: Chuanyan
  - family: Borné
    given: Yan
  - family: Gao
    given: Rui
  - family: López Rodriguez
    given: Maykel
  - family: Roell
    given: William C.
  - family: Wilson
    given: Jonathan M.
  - family: Regmi
    given: Ajit
  - family: Luan
    given: Cheng
  - family: Aly
    given: Dina Mansour
  - family: Peter
    given: Andreas
  - family: Machann
    given: Jürgen
  - family: Staiger
    given: Harald
  - family: Fritsche
    given: Andreas
  - family: Birkenfeld
    given: Andreas L.
  - family: Tao
    given: Rongya
  - family: Wagner
    given: Robert
  - family: Canouil
    given: Mickaël
  - family: Hong
    given: Mun-Gwan
  - family: Schwenk
    given: Jochen M.
  - family: Ahlqvist
    given: Emma
  - family: Kaikkonen
    given: Minna U.
  - family: Nilsson
    given: Peter
  - family: Shore
    given: Angela C.
  - family: Khan
    given: Faisel
  - family: Natali
    given: Andrea
  - family: Melander
    given: Olle
  - family: Orho-Melander
    given: Marju
  - family: Nilsson
    given: Jan
  - family: Häring
    given: Hans-Ulrich
  - family: Renström
    given: Erik
  - family: Wollheim
    given: Claes B.
  - family: Engström
    given: Gunnar
  - family: Weng
    given: Jianping
  - family: Pearson
    given: Ewan R.
  - family: Franks
    given: Paul W.
  - family: White
    given: Morris F.
  - family: Duffin
    given: Kevin L.
  - family: Vaag
    given: Allan Arthur
  - family: Laakso
    given: Markku
  - family: Stefan
    given: Norbert
  - family: Groop
    given: Leif
  - family: De Marinis
    given: Yang
  container-title: Nature Communications
  doi: 10.1038/s41467-021-26536-w
  id: wu_elevated_2021
  issn: 2041-1723
  issue: 1
  issued: 2021-11
  page: 6486
  title: Elevated circulating follistatin associates with an increased
    risk of type 2 diabetes
  type: article-journal
  url: "https://www.nature.com/articles/s41467-021-26536-w"
  volume: 12
  journal-title: '*Nature Communications*'
  date: 2021-11
  path: https://doi.org/10.1038/s41467-021-26536-w
  position: '17/42'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - family: Hegron
    given: Alan
  - family: Huh
    given: Eunna
  - family: Deupi
    given: Xavier
  - family: Sokrat
    given: Badr
  - family: Gao
    given: Wenwen
  - family: Le Gouill
    given: Christian
  - family: Canouil
    given: Mickaël
  - family: Boissel
    given: Mathilde
  - family: Charpentier
    given: Guillaume
  - family: Roussel
    given: Ronan
  - family: Balkau
    given: Beverley
  - family: Froguel
    given: Philippe
  - family: Plouffe
    given: Bianca
  - family: Bonnefond
    given: Amélie
  - family: Lichtarge
    given: Olivier
  - family: Jockers
    given: Ralf
  - family: Bouvier
    given: Michel
  container-title: ACS Pharmacology & Translational Science
  doi: 10.1021/acsptsci.1c00157
  id: hegron_identification_2021
  issn: 2575-9108, 2575-9108
  issue: 5
  issued: 2021-10
  page: 1614-1627
  title: Identification of Key Regions Mediating Human Melatonin Type 1
    Receptor Functional Selectivity Revealed by Natural Variants
  type: article-journal
  url: "https://pubs.acs.org/doi/10.1021/acsptsci.1c00157"
  volume: 4
  journal-title: '*ACS Pharmacology & Translational Science*'
  date: 2021-10
  path: https://doi.org/10.1021/acsptsci.1c00157
  position: '7/17'
  first: '&emsp;&emsp;&emsp;'
- abstract: OBJECTIVE Gestational diabetes mellitus (GDM) is associated
    with an increased risk of obesity and insulin resistance in
    offspring later in life, which might be explained by epigenetic
    changes in response to maternal hyperglycemic exposure.RESEARCH
    DESIGN AND METHODS We explored the association between GDM exposure
    and maternal blood and newborn cord blood methylation in 536
    mother-offspring pairs from the prospective FinnGeDi cohort using
    Illumina MethylationEPIC 850K BeadChip arrays. We assessed two
    hypotheses. First, we tested for shared maternal and offspring
    epigenetic effects resulting from GDM exposure. Second, we tested
    whether GDM exposure and maternal methylation had an epigenetic
    effect on the offspring.RESULTS We did not find any epigenetic marks
    (differentially methylated CpG probes) with shared and consistent
    effects between mothers and offspring. After including maternal
    methylation in the model, we identified a single significant (false
    discovery rate 1.38 × 10−2) CpG at the cg22790973 probe (TFCP2)
    associated with GDM. We identified seven additional FDR-significant
    interactions of maternal methylation and GDM status, with the
    strongest association at the same cg22790973 probe (TFCP2), as well
    as cg03456133, cg24440941 (H3C6), cg20002843 (LOC127841),
    cg19107264, and cg11493553 located within the UBE3C gene and
    cg17065901 in FAM13A, both susceptibility genes for type 2 diabetes
    and BMI, and cg23355087 within the DLGAP2 gene, known to be involved
    in insulin resistance during pregnancy.CONCLUSIONS Our study reveals
    the potential complexity of the epigenetic transmission between
    mothers with GDM and their offspring, likely determined by not only
    GDM exposure but also other factors indicated by maternal epigenetic
    status, such as maternal metabolic history.
  accessed: 2023-03-04
  annote: first
  author:
  - family: Canouil
    given: Mickaël
  - family: Khamis
    given: Amna
  - family: Keikkala
    given: Elina
  - family: Hummel
    given: Sandra
  - family: Lobbens
    given: Stephane
  - family: Bonnefond
    given: Amélie
  - family: Delahaye
    given: Fabien
  - family: Tzala
    given: Evangelia
  - family: Mustaniemi
    given: Sanna
  - family: Vääräsmäki
    given: Marja
  - family: Jarvelin
    given: Marjo-Riitta
  - family: Sebert
    given: Sylvain
  - family: Kajantie
    given: Eero
  - family: Froguel
    given: Philippe
  - family: Andrew
    given: Toby
  container-title: Diabetes Care
  doi: 10.2337/dc20-2960
  id: canouil_epigenome-wide_2021
  issn: 0149-5992, 1935-5548
  issue: 9
  issued: 2021-09
  page: 1992-1999
  title: Epigenome-Wide Association Study Reveals Methylation Loci
    Associated With Offspring Gestational Diabetes Mellitus Exposure and
    Maternal Methylome
  type: article-journal
  url: "https://diabetesjournals.org/care/article/44/9/1992/138857/Epigenome-Wide-Association-Study-Reveals"
  volume: 44
  journal-title: '*Diabetes Care*'
  date: 2021-09
  path: https://doi.org/10.2337/dc20-2960
  position: '1/15'
  first: '*As first or co-first*'
- abstract: Hyperactive SHP2 promotes inflammation-driven insulin
    resistance by skewing macrophage balance in metabolic tissues and
    may be a target in T2D. , Inflaming insulin resistancePatients with
    the developmental disorder Noonan syndrome (NS) may be prone to
    insulin resistance. Studying the hyperactivation of tyrosine
    phosphatase SHP2 associated with this disease, Paccoud et al . now
    pinpoint an inflammatory origin of insulin resistance.
    Hyperactivation of SHP2 associated with glucose intolerance and
    insulin resistance in patients with NS. In a hyperactive SHP2 mouse
    model, bone marrow--derived and liver-resident macrophages shifted
    toward a proinflammatory profile, leading to altered systemic
    glucose homeostasis. Small-molecule targeting of SHP2 in wild-type
    diet-induced obese mice reduced inflammation in metabolic tissues
    and improved insulin sensitivity, hinting at the potential of
    targeting SHP2 for metabolic syndrome., Insulin resistance is a key
    event in type 2 diabetes onset and a major comorbidity of obesity.
    It results from a combination of fat excess--triggered defects,
    including lipotoxicity and metaflammation, but the causal mechanisms
    remain difficult to identify. Here, we report that hyperactivation
    of the tyrosine phosphatase SHP2 found in Noonan syndrome (NS) led
    to an unsuspected insulin resistance profile uncoupled from altered
    lipid management (for example, obesity or ectopic lipid deposits) in
    both patients and mice. Functional exploration of an NS mouse model
    revealed this insulin resistance phenotype correlated with
    constitutive inflammation of tissues involved in the regulation of
    glucose metabolism. Bone marrow transplantation and macrophage
    depletion improved glucose homeostasis and decreased metaflammation
    in the mice, highlighting a key role of macrophages. In-depth
    analysis of bone marrow--derived macrophages in vitro and liver
    macrophages showed that hyperactive SHP2 promoted a proinflammatory
    phenotype, modified resident macrophage homeostasis, and triggered
    monocyte infiltration. Consistent with a role of SHP2 in promoting
    inflammation-driven insulin resistance, pharmaceutical SHP2
    inhibition in obese diabetic mice improved insulin sensitivity even
    better than conventional antidiabetic molecules by specifically
    reducing metaflammation and alleviating macrophage activation.
    Together, these results reveal that SHP2 hyperactivation leads to
    inflammation-triggered metabolic impairments and highlight the
    therapeutical potential of SHP2 inhibition to ameliorate insulin
    resistance.
  accessed: 2023-03-04
  author:
  - family: Paccoud
    given: Romain
  - family: Saint-Laurent
    given: Céline
  - family: Piccolo
    given: Enzo
  - family: Tajan
    given: Mylène
  - family: Dortignac
    given: Alizée
  - family: Pereira
    given: Ophélie
  - family: Le Gonidec
    given: Sophie
  - family: Baba
    given: Inès
  - family: Gélineau
    given: Adélaïde
  - family: Askia
    given: Haoussa
  - family: Branchereau
    given: Maxime
  - family: Charpentier
    given: Julie
  - family: Personnaz
    given: Jean
  - family: Branka
    given: Sophie
  - family: Auriau
    given: Johanna
  - family: Deleruyelle
    given: Simon
  - family: Canouil
    given: Mickaël
  - family: Beton
    given: Nicolas
  - family: Salles
    given: Jean-Pierre
  - family: Tauber
    given: Maithé
  - family: Weill
    given: Jacques
  - family: Froguel
    given: Philippe
  - family: Neel
    given: Benjamin G.
  - family: Araki
    given: Toshiyuki
  - family: Heymes
    given: Christophe
  - family: Burcelin
    given: Rémy
  - family: Castan
    given: Isabelle
  - family: Valet
    given: Philippe
  - family: Dray
    given: Cédric
  - family: Gautier
    given: Emmanuel L.
  - family: Edouard
    given: Thomas
  - family: Pradère
    given: Jean-Philippe
  - family: Yart
    given: Armelle
  container-title: Science Translational Medicine
  doi: 10.1126/scitranslmed.abe2587
  id: paccoud_shp2_2021
  issn: 1946-6234, 1946-6242
  issue: 591
  issued: 2021-04
  page: eabe2587
  title: SHP2 drives inflammation-triggered insulin resistance by
    reshaping tissue macrophage populations
  type: article-journal
  url: "https://www.science.org/doi/10.1126/scitranslmed.abe2587"
  volume: 13
  journal-title: '*Science Translational Medicine*'
  date: 2021-04
  path: https://doi.org/10.1126/scitranslmed.abe2587
  position: '17/33'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - family: Hu
    given: Ming
  - family: Cebola
    given: Inês
  - family: Carrat
    given: Gaelle
  - family: Jiang
    given: Shuying
  - family: Nawaz
    given: Sameena
  - family: Khamis
    given: Amna
  - family: Canouil
    given: Mickaël
  - family: Froguel
    given: Philippe
  - family: Schulte
    given: Anke
  - family: Solimena
    given: Michele
  - family: Ibberson
    given: Mark
  - family: Marchetti
    given: Piero
  - family: Cardenas-Diaz
    given: Fabian L.
  - family: Gadue
    given: Paul J.
  - family: Hastoy
    given: Benoit
  - family: Almeida-Souza
    given: Leonardo
  - family: McMahon
    given: Harvey
  - family: Rutter
    given: Guy A.
  container-title: Cell Reports
  doi: 10.1016/j.celrep.2021.108703
  id: hu_chromatin_2021
  issn: 22111247
  issue: 5
  issued: 2021-02
  page: 108703
  title: Chromatin 3D interaction analysis of the STARD10 locus unveils
    FCHSD2 as a regulator of insulin secretion
  type: article-journal
  url: "https://linkinghub.elsevier.com/retrieve/pii/S2211124721000164"
  volume: 34
  journal-title: '*Cell Reports*'
  date: 2021-02
  path: https://doi.org/10.1016/j.celrep.2021.108703
  position: '7/18'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - family: Marselli
    given: Lorella
  - family: Piron
    given: Anthony
  - family: Suleiman
    given: Mara
  - family: Colli
    given: Maikel L.
  - family: Yi
    given: Xiaoyan
  - family: Khamis
    given: Amna
  - family: Carrat
    given: Gaelle R.
  - family: Rutter
    given: Guy A.
  - family: Bugliani
    given: Marco
  - family: Giusti
    given: Laura
  - family: Ronci
    given: Maurizio
  - family: Ibberson
    given: Mark
  - family: Turatsinze
    given: Jean-Valery
  - family: Boggi
    given: Ugo
  - family: De Simone
    given: Paolo
  - family: De Tata
    given: Vincenzo
  - family: Lopes
    given: Miguel
  - family: Nasteska
    given: Daniela
  - family: De Luca
    given: Carmela
  - family: Tesi
    given: Marta
  - family: Bosi
    given: Emanuele
  - family: Singh
    given: Pratibha
  - family: Campani
    given: Daniela
  - family: Schulte
    given: Anke M.
  - family: Solimena
    given: Michele
  - family: Hecht
    given: Peter
  - family: Rady
    given: Brian
  - family: Bakaj
    given: Ivona
  - family: Pocai
    given: Alessandro
  - family: Norquay
    given: Lisa
  - family: Thorens
    given: Bernard
  - family: Canouil
    given: Mickaël
  - family: Froguel
    given: Philippe
  - family: Eizirik
    given: Decio L.
  - family: Cnop
    given: Miriam
  - family: Marchetti
    given: Piero
  container-title: Cell Reports
  doi: 10.1016/j.celrep.2020.108466
  id: marselli_persistent_2020
  issn: 22111247
  issue: 9
  issued: 2020-12
  page: 108466
  title: "Persistent or Transient Human β Cell Dysfunction Induced by
    Metabolic Stress: Specific Signatures and Shared Gene Expression
    with Type 2 Diabetes"
  title-short: Persistent or Transient Human β Cell Dysfunction Induced
    by Metabolic Stress
  type: article-journal
  url: "https://linkinghub.elsevier.com/retrieve/pii/S2211124720314558"
  volume: 33
  journal-title: '*Cell Reports*'
  date: 2020-12
  path: https://doi.org/10.1016/j.celrep.2020.108466
  position: '32/36'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - family: Vaxillaire
    given: Martine
  - family: Bonnefond
    given: Amélie
  - family: Liatis
    given: Stavros
  - family: Ben Salem Hachmi
    given: Leila
  - family: Jotic
    given: Aleksandra
  - family: Boissel
    given: Mathilde
  - family: Gaget
    given: Stefan
  - family: Durand
    given: Emmanuelle
  - family: Vaillant
    given: Emmanuel
  - family: Derhourhi
    given: Mehdi
  - family: Canouil
    given: Mickaël
  - family: Larcher
    given: Nicolas
  - family: Allegaert
    given: Frédéric
  - family: Medlej
    given: Rita
  - family: Chadli
    given: Asma
  - family: Belhadj
    given: Azzedine
  - family: Chaieb
    given: Molka
  - family: Raposo
    given: Joao-Felipe
  - family: Ilkova
    given: Hasan
  - family: Loizou
    given: Doros
  - family: Lalic
    given: Nebojsa
  - family: Vassallo
    given: Josanne
  - family: Marre
    given: Michel
  - family: Froguel
    given: Philippe
  container-title: Diabetes Research and Clinical Practice
  doi: 10.1016/j.diabres.2020.108553
  id: vaxillaire_monogenic_2021
  issn: 01688227
  issued: 2021-01
  page: 108553
  title: Monogenic diabetes characteristics in a transnational
    multicenter study from Mediterranean countries
  type: article-journal
  url: "https://linkinghub.elsevier.com/retrieve/pii/S016882272030810X"
  volume: 171
  journal-title: '*Diabetes Research and Clinical Practice*'
  date: 2021-01
  path: https://doi.org/10.1016/j.diabres.2020.108553
  position: '11/24'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - family: Bonnefond
    given: Amélie
  - family: Boissel
    given: Mathilde
  - family: Bolze
    given: Alexandre
  - family: Durand
    given: Emmanuelle
  - family: Toussaint
    given: Bénédicte
  - family: Vaillant
    given: Emmanuel
  - family: Gaget
    given: Stefan
  - family: Graeve
    given: Franck De
  - family: Dechaume
    given: Aurélie
  - family: Allegaert
    given: Frédéric
  - family: Guilcher
    given: David Le
  - family: Yengo
    given: Loïc
  - family: Dhennin
    given: Véronique
  - family: Borys
    given: Jean-Michel
  - family: Lu
    given: James T.
  - family: Cirulli
    given: Elizabeth T.
  - family: Elhanan
    given: Gai
  - family: Roussel
    given: Ronan
  - family: Balkau
    given: Beverley
  - family: Marre
    given: Michel
  - family: Franc
    given: Sylvia
  - family: Charpentier
    given: Guillaume
  - family: Vaxillaire
    given: Martine
  - family: Canouil
    given: Mickaël
  - family: Washington
    given: Nicole L.
  - family: Grzymski
    given: Joseph J.
  - family: Froguel
    given: Philippe
  container-title: Nature Metabolism
  doi: 10.1038/s42255-020-00294-3
  id: bonnefond_pathogenic_2020
  issn: 2522-5812
  issue: 10
  issued: 2020-10
  page: 1126-1134
  title: Pathogenic variants in actionable MODY genes are associated
    with type 2 diabetes
  type: article-journal
  url: "https://www.nature.com/articles/s42255-020-00294-3"
  volume: 2
  journal-title: '*Nature Metabolism*'
  date: 2020-10
  path: https://doi.org/10.1038/s42255-020-00294-3
  position: '24/27'
  first: '&emsp;&emsp;&emsp;'
- abstract: AbstractBackground Adipogenesis, the process whereby
    preadipocytes differentiate into mature adipocytes, is crucial for
    maintaining metabolic homeostasis. Cholesterol-lowering statins
    increase type 2 diabetes (T2D) risk possibly by affecting
    adipogenesis and insulin resistance but the (epi)genetic mechanisms
    involved are unknown. Here, we characterised the effects of statin
    treatment on adipocyte differentiation using in vitro human
    preadipocyte cell model to identify putative effective
    genes.ResultsStatin treatment during adipocyte differentiation
    caused a reduction in key genes involved in adipogenesis, such as
    ADIPOQ , GLUT4 and ABCG1. Using Illumina's Infinium '850K'850K
    Methylation EPIC array, we found a significant hypomethylation of
    cg14566882, located in the promoter of the histone deacetylase 9 (
    HDAC9) gene, in response to two types of statins (atorvastatin and
    mevastatin), which correlates with an increased HDAC9 mRNA
    expression. We confirmed that HDAC9 is a transcriptional repressor
    of the cholesterol efflux ABCG1 gene expression, which is
    epigenetically modified in obesity and prediabetic states. Thus, we
    assessed the putative impact of ABCG1 knockdown in mimicking the
    effect of statin in adipogenesis. ABCG1 KD reduced the expression of
    key genes involved in adipocyte differentiation and decreased
    insulin signalling and glucose uptake. In human blood cells from two
    cohorts, ABCG1 expression was impaired in response to statins,
    confirming that ABCG1 is targeted in vivo by these drugs.Conclusions
    We identified an epigenetic link between adipogenesis and adipose
    tissue insulin resistance in the context of T2D risk associated with
    statin use, which has important implications as HDAC9 and ABCG1 are
    considered potential therapeutic targets for obesity and metabolic
    diseases.
  accessed: 2023-03-04
  author:
  - family: Khamis
    given: Amna
  - family: Boutry
    given: Raphael
  - family: Canouil
    given: Mickaël
  - family: Mathew
    given: Sumi
  - family: Lobbens
    given: Stephane
  - family: Crouch
    given: Hutokshi
  - family: Andrew
    given: Toby
  - family: Abderrahmani
    given: Amar
  - family: Tamanini
    given: Filippo
  - family: Froguel
    given: Philippe
  container-title: Clinical Epigenetics
  doi: 10.1186/s13148-020-00858-w
  id: khamis_histone_2020
  issn: 1868-7075, 1868-7083
  issue: 1
  issued: 2020-12
  page: 68
  title: Histone deacetylase 9 promoter hypomethylation associated with
    adipocyte dysfunction is a statin-related metabolic effect
  type: article-journal
  url: "https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-020-00858-w"
  volume: 12
  journal-title: '*Clinical Epigenetics*'
  date: 2020-12
  path: https://doi.org/10.1186/s13148-020-00858-w
  position: '3/10'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - dropping-particle: de las
    family: Fuentes
    given: Lisa
  - family: Sung
    given: Yun Ju
  - family: Noordam
    given: Raymond
  - family: Winkler
    given: Thomas
  - family: Feitosa
    given: Mary F.
  - family: Schwander
    given: Karen
  - family: Bentley
    given: Amy R.
  - family: Brown
    given: Michael R.
  - family: Guo
    given: Xiuqing
  - family: Manning
    given: Alisa
  - family: Chasman
    given: Daniel I.
  - family: Aschard
    given: Hugues
  - family: Bartz
    given: Traci M.
  - family: Bielak
    given: Lawrence F.
  - family: Campbell
    given: Archie
  - family: Cheng
    given: Ching-Yu
  - family: Dorajoo
    given: Rajkumar
  - family: Hartwig
    given: Fernando P.
  - family: Horimoto
    given: A. R. V. R.
  - family: Li
    given: Changwei
  - family: Li-Gao
    given: Ruifang
  - family: Liu
    given: Yongmei
  - family: Marten
    given: Jonathan
  - family: Musani
    given: Solomon K.
  - family: Ntalla
    given: Ioanna
  - family: Rankinen
    given: Tuomo
  - family: Richard
    given: Melissa
  - family: Sim
    given: Xueling
  - family: Smith
    given: Albert V.
  - family: Tajuddin
    given: Salman M.
  - family: Tayo
    given: Bamidele O.
  - family: Vojinovic
    given: Dina
  - family: Warren
    given: Helen R.
  - family: Xuan
    given: Deng
  - family: Alver
    given: Maris
  - family: Boissel
    given: Mathilde
  - family: Chai
    given: Jin-Fang
  - family: Chen
    given: Xu
  - family: Christensen
    given: Kaare
  - family: Divers
    given: Jasmin
  - family: Evangelou
    given: Evangelos
  - family: Gao
    given: Chuan
  - family: Girotto
    given: Giorgia
  - family: Harris
    given: Sarah E.
  - family: He
    given: Meian
  - family: Hsu
    given: Fang-Chi
  - family: Kühnel
    given: Brigitte
  - family: Laguzzi
    given: Federica
  - family: Li
    given: Xiaoyin
  - family: Lyytikäinen
    given: Leo-Pekka
  - family: Nolte
    given: Ilja M.
  - family: Poveda
    given: Alaitz
  - family: Rauramaa
    given: Rainer
  - family: Riaz
    given: Muhammad
  - family: Rueedi
    given: Rico
  - family: Shu
    given: Xiao-ou
  - family: Snieder
    given: Harold
  - family: Sofer
    given: Tamar
  - family: Takeuchi
    given: Fumihiko
  - family: Verweij
    given: Niek
  - family: Ware
    given: Erin B.
  - family: Weiss
    given: Stefan
  - family: Yanek
    given: Lisa R.
  - family: Amin
    given: Najaf
  - family: Arking
    given: Dan E.
  - family: Arnett
    given: Donna K.
  - family: Bergmann
    given: Sven
  - family: Boerwinkle
    given: Eric
  - family: Brody
    given: Jennifer A.
  - family: Broeckel
    given: Ulrich
  - family: Brumat
    given: Marco
  - family: Burke
    given: Gregory
  - family: Cabrera
    given: Claudia P.
  - family: Canouil
    given: Mickaël
  - family: Chee
    given: Miao Li
  - family: Chen
    given: Yii-Der Ida
  - family: Cocca
    given: Massimiliano
  - family: Connell
    given: John
  - dropping-particle: de
    family: Silva
    given: H. Janaka
  - dropping-particle: de
    family: Vries
    given: Paul S.
  - family: Eiriksdottir
    given: Gudny
  - family: Faul
    given: Jessica D.
  - family: Fisher
    given: Virginia
  - family: Forrester
    given: Terrence
  - family: Fox
    given: Ervin F.
  - family: Friedlander
    given: Yechiel
  - family: Gao
    given: He
  - family: Gigante
    given: Bruna
  - family: Giulianini
    given: Franco
  - family: Gu
    given: Chi Charles
  - family: Gu
    given: Dongfeng
  - family: Harris
    given: Tamara B.
  - family: He
    given: Jiang
  - family: Heikkinen
    given: Sami
  - family: Heng
    given: Chew-Kiat
  - family: Hunt
    given: Steven
  - family: Ikram
    given: M. Arfan
  - family: Irvin
    given: Marguerite R.
  - family: Kähönen
    given: Mika
  - family: Kavousi
    given: Maryam
  - family: Khor
    given: Chiea Chuen
  - family: Kilpeläinen
    given: Tuomas O.
  - family: Koh
    given: Woon-Puay
  - family: Komulainen
    given: Pirjo
  - family: Kraja
    given: Aldi T.
  - family: Krieger
    given: J. E.
  - family: Langefeld
    given: Carl D.
  - family: Li
    given: Yize
  - family: Liang
    given: Jingjing
  - family: Liewald
    given: David C. M.
  - family: Liu
    given: Ching-Ti
  - family: Liu
    given: Jianjun
  - family: Lohman
    given: Kurt K.
  - family: Mägi
    given: Reedik
  - family: McKenzie
    given: Colin A.
  - family: Meitinger
    given: Thomas
  - family: Metspalu
    given: Andres
  - family: Milaneschi
    given: Yuri
  - family: Milani
    given: Lili
  - family: Mook-Kanamori
    given: Dennis O.
  - family: Nalls
    given: Mike A.
  - family: Nelson
    given: Christopher P.
  - family: Norris
    given: Jill M.
  - family: O'Connell
    given: Jeff
  - family: Ogunniyi
    given: Adesola
  - family: Padmanabhan
    given: Sandosh
  - family: Palmer
    given: Nicholette D.
  - family: Pedersen
    given: Nancy L.
  - family: Perls
    given: Thomas
  - family: Peters
    given: Annette
  - family: Petersmann
    given: Astrid
  - family: Peyser
    given: Patricia A.
  - family: Polasek
    given: Ozren
  - family: Porteous
    given: David J.
  - family: Raffel
    given: Leslie J.
  - family: Rice
    given: Treva K.
  - family: Rotter
    given: Jerome I.
  - family: Rudan
    given: Igor
  - family: Rueda-Ochoa
    given: Oscar-Leonel
  - family: Sabanayagam
    given: Charumathi
  - family: Salako
    given: Babatunde L.
  - family: Schreiner
    given: Pamela J.
  - family: Shikany
    given: James M.
  - family: Sidney
    given: Stephen S.
  - family: Sims
    given: Mario
  - family: Sitlani
    given: Colleen M.
  - family: Smith
    given: Jennifer A.
  - family: Starr
    given: John M.
  - family: Strauch
    given: Konstantin
  - family: Swertz
    given: Morris A.
  - family: Teumer
    given: Alexander
  - family: Tham
    given: Yih Chung
  - family: Uitterlinden
    given: André G.
  - family: Vaidya
    given: Dhananjay
  - dropping-particle: van der
    family: Ende
    given: M. Yldau
  - family: Waldenberger
    given: Melanie
  - family: Wang
    given: Lihua
  - family: Wang
    given: Ya-Xing
  - family: Wei
    given: Wen-Bin
  - family: Weir
    given: David R.
  - family: Wen
    given: Wanqing
  - family: Yao
    given: Jie
  - family: Yu
    given: Bing
  - family: Yu
    given: Caizheng
  - family: Yuan
    given: Jian-Min
  - family: Zhao
    given: Wei
  - family: Zonderman
    given: Alan B.
  - family: Becker
    given: Diane M.
  - family: Bowden
    given: Donald W.
  - family: Deary
    given: Ian J.
  - family: Dörr
    given: Marcus
  - family: Esko
    given: Tõnu
  - family: Freedman
    given: Barry I.
  - family: Froguel
    given: Philippe
  - family: Gasparini
    given: Paolo
  - family: Gieger
    given: Christian
  - family: Jonas
    given: Jost Bruno
  - family: Kammerer
    given: Candace M.
  - family: Kato
    given: Norihiro
  - family: Lakka
    given: Timo A.
  - family: Leander
    given: Karin
  - family: Lehtimäki
    given: Terho
  - literal: Lifelines Cohort Study
  - family: Magnusson
    given: Patrik K. E.
  - family: Marques-Vidal
    given: Pedro
  - family: Penninx
    given: Brenda W. J. H.
  - family: Samani
    given: Nilesh J.
  - dropping-particle: van der
    family: Harst
    given: Pim
  - family: Wagenknecht
    given: Lynne E.
  - family: Wu
    given: Tangchun
  - family: Zheng
    given: Wei
  - family: Zhu
    given: Xiaofeng
  - family: Bouchard
    given: Claude
  - family: Cooper
    given: Richard S.
  - family: Correa
    given: Adolfo
  - family: Evans
    given: Michele K.
  - family: Gudnason
    given: Vilmundur
  - family: Hayward
    given: Caroline
  - family: Horta
    given: Bernardo L.
  - family: Kelly
    given: Tanika N.
  - family: Kritchevsky
    given: Stephen B.
  - family: Levy
    given: Daniel
  - family: Palmas
    given: Walter R.
  - family: Pereira
    given: A. C.
  - family: Province
    given: Michael M.
  - family: Psaty
    given: Bruce M.
  - family: Ridker
    given: Paul M.
  - family: Rotimi
    given: Charles N.
  - family: Tai
    given: E. Shyong
  - dropping-particle: van
    family: Dam
    given: Rob M.
  - dropping-particle: van
    family: Duijn
    given: Cornelia M.
  - family: Wong
    given: Tien Yin
  - family: Rice
    given: Kenneth
  - family: Gauderman
    given: W. James
  - family: Morrison
    given: Alanna C.
  - family: North
    given: Kari E.
  - family: Kardia
    given: Sharon L. R.
  - family: Caulfield
    given: Mark J.
  - family: Elliott
    given: Paul
  - family: Munroe
    given: Patricia B.
  - family: Franks
    given: Paul W.
  - family: Rao
    given: Dabeeru C.
  - family: Fornage
    given: Myriam
  container-title: Molecular Psychiatry
  doi: 10.1038/s41380-020-0719-3
  id: de_las_fuentes_gene-educational_2021
  issn: 1359-4184, 1476-5578
  issue: 6
  issued: 2021-06
  page: 2111-2125
  title: Gene-educational attainment interactions in a multi-ancestry
    genome-wide meta-analysis identify novel blood pressure loci
  type: article-journal
  url: "https://www.nature.com/articles/s41380-020-0719-3"
  volume: 26
  journal-title: '*Molecular Psychiatry*'
  date: 2021-06
  path: https://doi.org/10.1038/s41380-020-0719-3
  position: '73/215'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - family: Gloaguen
    given: Emilie
  - family: Dizier
    given: Marie‐Hélène
  - family: Boissel
    given: Mathilde
  - family: Rocheleau
    given: Ghislain
  - family: Canouil
    given: Mickaël
  - family: Froguel
    given: Philippe
  - family: Tichet
    given: Jean
  - family: Roussel
    given: Ronan
  - literal: The D.E.S.I.R. Study Group
  - family: Julier
    given: Cécile
  - family: Balkau
    given: Beverley
  - family: Mathieu
    given: Flavie
  container-title: Annals of Human Genetics
  doi: 10.1111/ahg.12372
  id: gloaguen_general_2020
  issn: 0003-4800, 1469-1809
  issue: 3
  issued: 2020-05
  page: 280-290
  title: "General regression model: A \"model‐free\" association test for
    quantitative traits allowing to test for the underlying genetic
    model"
  title-short: General regression model
  type: article-journal
  url: "https://onlinelibrary.wiley.com/doi/10.1111/ahg.12372"
  volume: 84
  journal-title: '*Annals of Human Genetics*'
  date: 2020-05
  path: https://doi.org/10.1111/ahg.12372
  position: '5/11'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - family: Baron
    given: Morgane
  - family: Maillet
    given: Julie
  - family: Huyvaert
    given: Marlène
  - family: Dechaume
    given: Aurélie
  - family: Boutry
    given: Raphaël
  - family: Loiselle
    given: Hélène
  - family: Durand
    given: Emmanuelle
  - family: Toussaint
    given: Bénédicte
  - family: Vaillant
    given: Emmanuel
  - family: Philippe
    given: Julien
  - family: Thomas
    given: Jérémy
  - family: Ghulam
    given: Amjad
  - family: Franc
    given: Sylvia
  - family: Charpentier
    given: Guillaume
  - family: Borys
    given: Jean-Michel
  - family: Lévy-Marchal
    given: Claire
  - family: Tauber
    given: Maïthé
  - family: Scharfmann
    given: Raphaël
  - family: Weill
    given: Jacques
  - family: Aubert
    given: Cécile
  - family: Kerr-Conte
    given: Julie
  - family: Pattou
    given: François
  - family: Roussel
    given: Ronan
  - family: Balkau
    given: Beverley
  - family: Marre
    given: Michel
  - family: Boissel
    given: Mathilde
  - family: Derhourhi
    given: Mehdi
  - family: Gaget
    given: Stefan
  - family: Canouil
    given: Mickaël
  - family: Froguel
    given: Philippe
  - family: Bonnefond
    given: Amélie
  container-title: Nature Medicine
  doi: 10.1038/s41591-019-0622-0
  id: baron_loss\--function_2019
  issn: 1078-8956, 1546-170X
  issue: 11
  issued: 2019-11
  page: 1733-1738
  title: Loss-of-function mutations in MRAP2 are pathogenic in
    hyperphagic obesity with hyperglycemia and hypertension
  type: article-journal
  url: "http://www.nature.com/articles/s41591-019-0622-0"
  volume: 25
  journal-title: '*Nature Medicine*'
  date: 2019-11
  path: https://doi.org/10.1038/s41591-019-0622-0
  position: '29/31'
  first: '&emsp;&emsp;&emsp;'
- abstract: "AbstractSummary The NanoStringTM nCounter® is a platform
    for the targeted quantification of expression data in biofluids and
    tissues. While software by the manufacturer is available in addition
    to third parties packages, they do not provide a complete quality
    control (QC) pipeline. Here, we present NACHO ('NAnostring quality
    Control dasHbOard'NAnostring quality Control dasHbOard), a
    comprehensive QC R-package. The package consists of three subsequent
    steps: summarize, visualize and normalize. The summarize function
    collects all the relevant data and stores it in a tidy format, the
    visualize function initiates a dashboard with plots of the relevant
    QC outcomes. It contains QC metrics that are measured by default by
    the manufacturer, but also calculates other insightful measures,
    including the scaling factors that are needed in the normalization
    step. In this normalization step, different normalization methods
    can be chosen to optimally preprocess data. Together, NACHO is a
    comprehensive method that optimizes insight and preprocessing of
    nCounter® data.Availability and implementation NACHO is available as
    an R-package on CRAN and the development version on GitHub
    https://github.com/mcanouil/NACHO.Supplementary information
    Supplementary data are available at Bioinformatics online."
  accessed: 2023-03-04
  annote: first
  author:
  - family: Canouil
    given: Mickaël
  - family: Bouland
    given: Gerard A
  - family: Bonnefond
    given: Amélie
  - family: Froguel
    given: Philippe
  - dropping-particle: "'t"
    family: Hart
    given: Leen M
  - family: Slieker
    given: Roderick C
  container-title: Bioinformatics
  doi: 10.1093/bioinformatics/btz647
  editor:
  - family: Wren
    given: Jonathan
  id: canouil_nacho_2020
  issn: 1367-4803, 1367-4811
  issue: 3
  issued: 2020-02
  page: 970-971
  title: "*NACHO:* An R package for quality control of NanoString
    [nCounter]{.nocase} data"
  title-short: \<I\>NACHO
  type: article-journal
  url: "https://academic.oup.com/bioinformatics/article/36/3/970/5553566"
  volume: 36
  journal-title: '*Bioinformatics*'
  date: 2020-02
  path: https://doi.org/10.1093/bioinformatics/btz647
  position: '1/6'
  first: '*As first or co-first*'
- accessed: 2023-03-04
  author:
  - family: Ndiaye
    given: Fatou K.
  - family: Huyvaert
    given: Marlène
  - family: Ortalli
    given: Ana
  - family: Canouil
    given: Mickaël
  - family: Lecoeur
    given: Cécile
  - family: Verbanck
    given: Marie
  - family: Lobbens
    given: Stéphane
  - family: Khamis
    given: Amna
  - family: Marselli
    given: Lorella
  - family: Marchetti
    given: Piero
  - family: Kerr-Conte
    given: Julie
  - family: Pattou
    given: François
  - family: Marre
    given: Michel
  - family: Roussel
    given: Ronan
  - family: Balkau
    given: Beverley
  - family: Froguel
    given: Philippe
  - family: Bonnefond
    given: Amélie
  container-title: International Journal of Obesity
  doi: 10.1038/s41366-019-0428-7
  id: ndiaye_expression_2020
  issn: 0307-0565, 1476-5497
  issue: 2
  issued: 2020-02
  page: 539-543
  title: The expression of genes in top obesity-associated loci is
    enriched in insula and substantia nigra brain regions involved in
    addiction and reward
  type: article-journal
  url: "http://www.nature.com/articles/s41366-019-0428-7"
  volume: 44
  journal-title: '*International Journal of Obesity*'
  date: 2020-02
  path: https://doi.org/10.1038/s41366-019-0428-7
  position: '4/17'
  first: '&emsp;&emsp;&emsp;'
- abstract: Abstract Although hundreds of genome-wide association
    studies-implicated loci have been reported for adult obesity-related
    traits, less is known about the genetics specific for early-onset
    obesity and with only a few studies conducted in non-European
    populations to date. Searching for additional genetic variants
    associated with childhood obesity, we performed a trans-ancestral
    meta-analysis of 30 studies consisting of up to 13 005 cases (≥95th
    percentile of body mass index (BMI) achieved 2--18 years old) and
    15 599 controls (consistently &lt;50th percentile of BMI) of
    European, African, North/South American and East Asian ancestry.
    Suggestive loci were taken forward for replication in a sample of
    1888 cases and 4689 controls from seven cohorts of European and
    North/South American ancestry. In addition to observing 18
    previously implicated BMI or obesity loci, for both early and late
    onset, we uncovered one completely novel locus in this
    trans-ancestral analysis (nearest gene, METTL15). The variant was
    nominally associated with only the European subgroup analysis but
    had a consistent direction of effect in other ethnicities. We then
    utilized trans-ancestral Bayesian analysis to narrow down the
    location of the probable causal variant at each genome-wide
    significant signal. Of all the fine-mapped loci, we were able to
    narrow down the causative variant at four known loci to fewer than
    10 single nucleotide polymorphisms (SNPs) (FAIM2, GNPDA2, MC4R and
    SEC16B loci). In conclusion, an ethnically diverse setting has
    enabled us to both identify an additional pediatric obesity locus
    and further fine-map existing loci.
  accessed: 2023-03-04
  author:
  - family: Bradfield
    given: Jonathan P
  - family: Vogelezang
    given: Suzanne
  - family: Felix
    given: Janine F
  - family: Chesi
    given: Alessandra
  - family: Helgeland
    given: Øyvind
  - family: Horikoshi
    given: Momoko
  - family: Karhunen
    given: Ville
  - family: Lowry
    given: Estelle
  - family: Cousminer
    given: Diana L
  - family: Ahluwalia
    given: Tarunveer S
  - family: Thiering
    given: Elisabeth
  - family: Boh
    given: Eileen Tai-Hui
  - family: Zafarmand
    given: Mohammad H
  - family: Vilor-Tejedor
    given: Natalia
  - family: Wang
    given: Carol A
  - family: Joro
    given: Raimo
  - family: Chen
    given: Zhanghua
  - family: Gauderman
    given: William J
  - family: Pitkänen
    given: Niina
  - family: Parra
    given: Esteban J
  - family: Fernandez-Rhodes
    given: Lindsay
  - family: Alyass
    given: Akram
  - family: Monnereau
    given: Claire
  - family: Curtin
    given: John A
  - family: Have
    given: Christian T
  - family: McCormack
    given: Shana E
  - family: Hollensted
    given: Mette
  - family: Frithioff-Bøjsøe
    given: Christine
  - family: Valladares-Salgado
    given: Adan
  - family: Peralta-Romero
    given: Jesus
  - family: Teo
    given: Yik-Ying
  - family: Standl
    given: Marie
  - family: Leinonen
    given: Jaakko T
  - family: Holm
    given: Jens-Christian
  - family: Peters
    given: Triinu
  - family: Vioque
    given: Jesus
  - family: Vrijheid
    given: Martine
  - family: Simpson
    given: Angela
  - family: Custovic
    given: Adnan
  - family: Vaudel
    given: Marc
  - family: Canouil
    given: Mickaël
  - family: Lindi
    given: Virpi
  - family: Atalay
    given: Mustafa
  - family: Kähönen
    given: Mika
  - family: Raitakari
    given: Olli T
  - dropping-particle: van
    family: Schaik
    given: Barbera D C
  - family: Berkowitz
    given: Robert I
  - family: Cole
    given: Shelley A
  - family: Voruganti
    given: V Saroja
  - family: Wang
    given: Yujie
  - family: Highland
    given: Heather M
  - family: Comuzzie
    given: Anthony G
  - family: Butte
    given: Nancy F
  - family: Justice
    given: Anne E
  - family: Gahagan
    given: Sheila
  - family: Blanco
    given: Estela
  - family: Lehtimäki
    given: Terho
  - family: Lakka
    given: Timo A
  - family: Hebebrand
    given: Johannes
  - family: Bonnefond
    given: Amélie
  - family: Grarup
    given: Niels
  - family: Froguel
    given: Philippe
  - family: Lyytikäinen
    given: Leo-Pekka
  - family: Cruz
    given: Miguel
  - family: Kobes
    given: Sayuko
  - family: Hanson
    given: Robert L
  - family: Zemel
    given: Babette S
  - family: Hinney
    given: Anke
  - family: Teo
    given: Koon K
  - family: Meyre
    given: David
  - family: North
    given: Kari E
  - family: Gilliland
    given: Frank D
  - family: Bisgaard
    given: Hans
  - family: Bustamante
    given: Mariona
  - family: Bonnelykke
    given: Klaus
  - family: Pennell
    given: Craig E
  - family: Rivadeneira
    given: Fernando
  - family: Uitterlinden
    given: André G
  - family: Baier
    given: Leslie J
  - family: Vrijkotte
    given: Tanja G M
  - family: Heinrich
    given: Joachim
  - family: Sørensen
    given: Thorkild I A
  - family: Saw
    given: Seang-Mei
  - family: Pedersen
    given: Oluf
  - family: Hansen
    given: Torben
  - family: Eriksson
    given: Johan
  - family: Widén
    given: Elisabeth
  - family: McCarthy
    given: Mark I
  - family: Njølstad
    given: Pål R
  - family: Power
    given: Christine
  - family: Hyppönen
    given: Elina
  - family: Sebert
    given: Sylvain
  - family: Brown
    given: Christopher D
  - family: Järvelin
    given: Marjo-Riitta
  - family: Timpson
    given: Nicholas J
  - family: Johansson
    given: Stefan
  - family: Hakonarson
    given: Hakon
  - family: Jaddoe
    given: Vincent W V
  - literal: Struan F A Grant for the Early Growth Genetics Consortium
  container-title: Human Molecular Genetics
  doi: 10.1093/hmg/ddz161
  id: bradfield_trans-ancestral_2019
  issn: 0964-6906, 1460-2083
  issue: 19
  issued: 2019-10
  page: 3327-3338
  title: A trans-ancestral meta-analysis of genome-wide association
    studies reveals loci associated with childhood obesity
  type: article-journal
  url: "https://academic.oup.com/hmg/article/28/19/3327/5528371"
  volume: 28
  journal-title: '*Human Molecular Genetics*'
  date: 2019-10
  path: https://doi.org/10.1093/hmg/ddz161
  position: '41/97'
  first: '&emsp;&emsp;&emsp;'
- abstract: AbstractType 2 diabetes (T2D) affects the health of millions
    of people worldwide. The identification of genetic determinants
    associated with changes in glycemia over time might illuminate
    biological features that precede the development of T2D. Here we
    conducted a genome-wide association study of longitudinal fasting
    glucose changes in up to 13,807 non-diabetic individuals of European
    descent from nine cohorts. Fasting glucose change over time was
    defined as the slope of the line defined by multiple fasting glucose
    measurements obtained over up to 14 years of observation. We tested
    for associations of genetic variants with inverse-normal transformed
    fasting glucose change over time adjusting for age at baseline, sex,
    and principal components of genetic variation. We found no
    genome-wide significant association (P \<\< 5 × 10 −8 ) with fasting
    glucose change over time. Seven loci previously associated with T2D,
    fasting glucose or HbA1c were nominally (P \<\< 0.05) associated
    with fasting glucose change over time. Limited power influences
    unambiguous interpretation, but these data suggest that genetic
    effects on fasting glucose change over time are likely to be small.
    A public version of the data provides a genomic resource to combine
    with future studies to evaluate shared genetic links with T2D and
    other metabolic risk traits.
  accessed: 2023-03-04
  author:
  - family: Liu
    given: Ching-Ti
  - family: Merino
    given: Jordi
  - family: Rybin
    given: Denis
  - family: DiCorpo
    given: Daniel
  - family: Benke
    given: Kelly S.
  - family: Bragg-Gresham
    given: Jennifer L.
  - family: Canouil
    given: Mickaël
  - family: Corre
    given: Tanguy
  - family: Grallert
    given: Harald
  - family: Isaacs
    given: Aaron
  - family: Kutalik
    given: Zoltan
  - family: Lahti
    given: Jari
  - family: Marullo
    given: Letizia
  - family: Marzi
    given: Carola
  - family: Rasmussen-Torvik
    given: Laura J.
  - family: Rocheleau
    given: Ghislain
  - family: Rueedi
    given: Rico
  - family: Scapoli
    given: Chiara
  - family: Verweij
    given: Niek
  - family: Vogelzangs
    given: Nicole
  - family: Willems
    given: Sara M.
  - family: Yengo
    given: Loïc
  - family: Bakker
    given: Stephan J. L.
  - family: Beilby
    given: John
  - family: Hui
    given: Jennie
  - family: Kajantie
    given: Eero
  - family: Müller-Nurasyid
    given: Martina
  - family: Rathmann
    given: Wolfgang
  - family: Balkau
    given: Beverley
  - family: Bergmann
    given: Sven
  - family: Eriksson
    given: Johan G.
  - family: Florez
    given: Jose C.
  - family: Froguel
    given: Philippe
  - family: Harris
    given: Tamara
  - family: Hung
    given: Joseph
  - family: James
    given: Alan L.
  - family: Kavousi
    given: Maryam
  - family: Miljkovic
    given: Iva
  - family: Musk
    given: Arthur W.
  - family: Palmer
    given: Lyle J.
  - family: Peters
    given: Annette
  - family: Roussel
    given: Ronan
  - dropping-particle: van der
    family: harst
    given: Pim
  - dropping-particle: van
    family: Duijn
    given: Cornelia M.
  - family: Vollenweider
    given: Peter
  - family: Barroso
    given: Inês
  - family: Prokopenko
    given: Inga
  - family: Dupuis
    given: Josée
  - family: Meigs
    given: James B.
  - family: Bouatia-Naji
    given: Nabila
  container-title: Scientific Reports
  doi: 10.1038/s41598-019-45823-7
  id: liu_genome-wide_2019
  issn: 2045-2322
  issue: 1
  issued: 2019-07
  page: 9439
  title: Genome-wide Association Study of Change in Fasting Glucose over
    time in 13,807 non-diabetic European Ancestry Individuals
  type: article-journal
  url: "https://www.nature.com/articles/s41598-019-45823-7"
  volume: 9
  journal-title: '*Scientific Reports*'
  date: 2019-07
  path: https://doi.org/10.1038/s41598-019-45823-7
  position: '7/48'
  first: '&emsp;&emsp;&emsp;'
- abstract: Abstract Elevated blood pressure (BP), a leading cause of
    global morbidity and mortality, is influenced by both genetic and
    lifestyle factors. Cigarette smoking is one such lifestyle factor.
    Across five ancestries, we performed a genome-wide gene--smoking
    interaction study of mean arterial pressure (MAP) and pulse pressure
    (PP) in 129 913 individuals in stage 1 and follow-up analysis in
    480 178 additional individuals in stage 2. We report here 136 loci
    significantly associated with MAP and/or PP. Of these, 61 were
    previously published through main-effect analysis of BP traits, 37
    were recently reported by us for systolic BP and/or diastolic BP
    through gene--smoking interaction analysis and 38 were newly
    identified (P \< 5 × 10−8, false discovery rate \< 0.05). We also
    identified nine new signals near known loci. Of the 136 loci, 8
    showed significant interaction with smoking status. They include
    CSMD1 previously reported for insulin resistance and BP in the
    spontaneously hypertensive rats. Many of the 38 new loci show
    biologic plausibility for a role in BP regulation. SLC26A7 encodes a
    chloride/bicarbonate exchanger expressed in the renal outer
    medullary collecting duct. AVPR1A is widely expressed, including in
    vascular smooth muscle cells, kidney, myocardium and brain. FHAD1 is
    a long non-coding RNA overexpressed in heart failure. TMEM51 was
    associated with contractile function in cardiomyocytes. CASP9 plays
    a central role in cardiomyocyte apoptosis. Identified only in
    African ancestry were 30 novel loci. Our findings highlight the
    value of multi-ancestry investigations, particularly in studies of
    interaction with lifestyle factors, where genomic and lifestyle
    differences may contribute to novel findings.
  accessed: 2023-03-04
  author:
  - family: Sung
    given: Yun Ju
  - dropping-particle: de las
    family: Fuentes
    given: Lisa
  - family: Winkler
    given: Thomas W
  - family: Chasman
    given: Daniel I
  - family: Bentley
    given: Amy R
  - family: Kraja
    given: Aldi T
  - family: Ntalla
    given: Ioanna
  - family: Warren
    given: Helen R
  - family: Guo
    given: Xiuqing
  - family: Schwander
    given: Karen
  - family: Manning
    given: Alisa K
  - family: Brown
    given: Michael R
  - family: Aschard
    given: Hugues
  - family: Feitosa
    given: Mary F
  - family: Franceschini
    given: Nora
  - family: Lu
    given: Yingchang
  - family: Cheng
    given: Ching-Yu
  - family: Sim
    given: Xueling
  - family: Vojinovic
    given: Dina
  - family: Marten
    given: Jonathan
  - family: Musani
    given: Solomon K
  - family: Kilpeläinen
    given: Tuomas O
  - family: Richard
    given: Melissa A
  - family: Aslibekyan
    given: Stella
  - family: Bartz
    given: Traci M
  - family: Dorajoo
    given: Rajkumar
  - family: Li
    given: Changwei
  - family: Liu
    given: Yongmei
  - family: Rankinen
    given: Tuomo
  - family: Smith
    given: Albert Vernon
  - family: Tajuddin
    given: Salman M
  - family: Tayo
    given: Bamidele O
  - family: Zhao
    given: Wei
  - family: Zhou
    given: Yanhua
  - family: Matoba
    given: Nana
  - family: Sofer
    given: Tamar
  - family: Alver
    given: Maris
  - family: Amini
    given: Marzyeh
  - family: Boissel
    given: Mathilde
  - family: Chai
    given: Jin Fang
  - family: Chen
    given: Xu
  - family: Divers
    given: Jasmin
  - family: Gandin
    given: Ilaria
  - family: Gao
    given: Chuan
  - family: Giulianini
    given: Franco
  - family: Goel
    given: Anuj
  - family: Harris
    given: Sarah E
  - family: Hartwig
    given: Fernando P
  - family: He
    given: Meian
  - family: Horimoto
    given: Andrea R V R
  - family: Hsu
    given: Fang-Chi
  - family: Jackson
    given: Anne U
  - family: Kammerer
    given: Candace M
  - family: Kasturiratne
    given: Anuradhani
  - family: Komulainen
    given: Pirjo
  - family: Kühnel
    given: Brigitte
  - family: Leander
    given: Karin
  - family: Lee
    given: Wen-Jane
  - family: Lin
    given: Keng-Hung
  - family: Luan
    given: Jian'an
  - family: Lyytikäinen
    given: Leo-Pekka
  - family: McKenzie
    given: Colin A
  - family: Nelson
    given: Christopher P
  - family: Noordam
    given: Raymond
  - family: Scott
    given: Robert A
  - family: Sheu
    given: Wayne H H
  - family: Stančáková
    given: Alena
  - family: Takeuchi
    given: Fumihiko
  - dropping-particle: van der
    family: Most
    given: Peter J
  - family: Varga
    given: Tibor V
  - family: Waken
    given: Robert J
  - family: Wang
    given: Heming
  - family: Wang
    given: Yajuan
  - family: Ware
    given: Erin B
  - family: Weiss
    given: Stefan
  - family: Wen
    given: Wanqing
  - family: Yanek
    given: Lisa R
  - family: Zhang
    given: Weihua
  - family: Zhao
    given: Jing Hua
  - family: Afaq
    given: Saima
  - family: Alfred
    given: Tamuno
  - family: Amin
    given: Najaf
  - family: Arking
    given: Dan E
  - family: Aung
    given: Tin
  - family: Barr
    given: R Graham
  - family: Bielak
    given: Lawrence F
  - family: Boerwinkle
    given: Eric
  - family: Bottinger
    given: Erwin P
  - family: Braund
    given: Peter S
  - family: Brody
    given: Jennifer A
  - family: Broeckel
    given: Ulrich
  - family: Cade
    given: Brian
  - family: Campbell
    given: Archie
  - family: Canouil
    given: Mickaël
  - family: Chakravarti
    given: Aravinda
  - family: Cocca
    given: Massimiliano
  - family: Collins
    given: Francis S
  - family: Connell
    given: John M
  - dropping-particle: de
    family: Mutsert
    given: Renée
  - dropping-particle: de
    family: Silva
    given: H Janaka
  - family: Dörr
    given: Marcus
  - family: Duan
    given: Qing
  - family: Eaton
    given: Charles B
  - family: Ehret
    given: Georg
  - family: Evangelou
    given: Evangelos
  - family: Faul
    given: Jessica D
  - family: Forouhi
    given: Nita G
  - family: Franco
    given: Oscar H
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  container-title: Human Molecular Genetics
  doi: 10.1093/hmg/ddz070
  id: sung_multi-ancestry_2019
  issn: 0964-6906, 1460-2083
  issue: 15
  issued: 2019-08
  page: 2615-2633
  title: A multi-ancestry genome-wide study incorporating gene--smoking
    interactions identifies multiple new loci for pulse pressure and
    mean arterial pressure
  type: article-journal
  url: "https://academic.oup.com/hmg/article/28/15/2615/5439584"
  volume: 28
  journal-title: '*Human Molecular Genetics*'
  date: 2019-08
  path: https://doi.org/10.1093/hmg/ddz070
  position: '92/273'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
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  - literal: COGENT-Kidney Consortium
  - literal: EPIC-InterAct Consortium
  - literal: Understanding Society Scientific Group
  - literal: Lifelines Cohort
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  container-title: Nature Genetics
  doi: 10.1038/s41588-019-0378-y
  id: cogent-kidney_consortium_multi-ancestry_2019
  issn: 1061-4036, 1546-1718
  issue: 4
  issued: 2019-04
  page: 636-648
  title: Multi-ancestry genome-wide gene--smoking interaction study of
    387,272 individuals identifies new loci associated with serum lipids
  type: article-journal
  url: "http://www.nature.com/articles/s41588-019-0378-y"
  volume: 51
  journal-title: '*Nature Genetics*'
  date: 2019-04
  path: https://doi.org/10.1038/s41588-019-0378-y
  position: '96/292'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  annote: first
  author:
  - family: Khamis
    given: Amna
  - family: Canouil
    given: Mickaël
  - family: Siddiq
    given: Afshan
  - family: Crouch
    given: Hutokshi
  - family: Falchi
    given: Mario
  - family: Bulow
    given: Manon von
  - family: Ehehalt
    given: Florian
  - family: Marselli
    given: Lorella
  - family: Distler
    given: Marius
  - family: Richter
    given: Daniela
  - family: Weitz
    given: Jürgen
  - family: Bokvist
    given: Krister
  - family: Xenarios
    given: Ioannis
  - family: Thorens
    given: Bernard
  - family: Schulte
    given: Anke M.
  - family: Ibberson
    given: Mark
  - family: Bonnefond
    given: Amelie
  - family: Marchetti
    given: Piero
  - family: Solimena
    given: Michele
  - family: Froguel
    given: Philippe
  container-title: Molecular Metabolism
  doi: 10.1016/j.molmet.2019.03.004
  id: khamis_laser_2019
  issn: 22128778
  issued: 2019-06
  page: 98-107
  title: Laser capture microdissection of human pancreatic islets
    reveals novel [eQTLs]{.nocase} associated with type 2 diabetes
  type: article-journal
  url: "https://linkinghub.elsevier.com/retrieve/pii/S2212877819301309"
  volume: 24
  journal-title: '*Molecular Metabolism*'
  date: 2019-06
  path: https://doi.org/10.1016/j.molmet.2019.03.004
  position: '2/20'
  first: '*As first or co-first*'
- accessed: 2023-03-04
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  - dropping-particle: de
    family: Vries
    given: Paul S
  - family: Brown
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  - family: Bentley
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  - family: Sung
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  - family: Winkler
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  - family: Ntalla
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  - family: Schwander
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  - family: Kraja
    given: Aldi T
  - family: Guo
    given: Xiuqing
  - family: Franceschini
    given: Nora
  - family: Cheng
    given: Ching-Yu
  - family: Sim
    given: Xueling
  - family: Vojinovic
    given: Dina
  - family: Huffman
    given: Jennifer E
  - family: Musani
    given: Solomon K
  - family: Li
    given: Changwei
  - family: Feitosa
    given: Mary F
  - family: Richard
    given: Melissa A
  - family: Noordam
    given: Raymond
  - family: Aschard
    given: Hugues
  - family: Bartz
    given: Traci M
  - family: Bielak
    given: Lawrence F
  - family: Deng
    given: Xuan
  - family: Dorajoo
    given: Rajkumar
  - family: Lohman
    given: Kurt K
  - family: Manning
    given: Alisa K
  - family: Rankinen
    given: Tuomo
  - family: Smith
    given: Albert V
  - family: Tajuddin
    given: Salman M
  - family: Evangelou
    given: Evangelos
  - family: Graff
    given: Mariaelisa
  - family: Alver
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  - family: Boissel
    given: Mathilde
  - family: Chai
    given: Jin Fang
  - family: Chen
    given: Xu
  - family: Divers
    given: Jasmin
  - family: Gandin
    given: Ilaria
  - family: Gao
    given: Chuan
  - family: Goel
    given: Anuj
  - family: Hagemeijer
    given: Yanick
  - family: Harris
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  - family: Hartwig
    given: Fernando P
  - family: He
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  - family: Horimoto
    given: Andrea R V R
  - family: Hsu
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  - family: Jackson
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  - family: Kasturiratne
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  - family: Komulainen
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  - family: Kühnel
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  - family: Laguzzi
    given: Federica
  - family: Lee
    given: Joseph H
  - family: Luan
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  - family: Lyytikäinen
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  - family: Matoba
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  - family: Nolte
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  - family: Pietzner
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  - family: Riaz
    given: Muhammad
  - family: Said
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  - family: Scott
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  - family: Sofer
    given: Tamar
  - family: Stančáková
    given: Alena
  - family: Takeuchi
    given: Fumihiko
  - family: Tayo
    given: Bamidele O
  - dropping-particle: van der
    family: Most
    given: Peter J
  - family: Varga
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  - family: Wang
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  - family: Ware
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  - family: Wen
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  - family: Yanek
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  - family: Zhang
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  - family: Zhao
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  - family: Afaq
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  - family: Amin
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  - family: Amini
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  - family: Arking
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  - family: Aung
    given: Tin
  - family: Ballantyne
    given: Christie
  - family: Boerwinkle
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  - family: Broeckel
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  - family: Campbell
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  - family: Canouil
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  - family: Charumathi
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  - family: Chen
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  - family: Connell
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  - dropping-particle: de
    family: Faire
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  - dropping-particle: de las
    family: Fuentes
    given: Lisa
  - dropping-particle: de
    family: Mutsert
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  - dropping-particle: de
    family: Silva
    given: H Janaka
  - family: Ding
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  - family: Dominiczak
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  - family: Duan
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  - family: Eaton
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  - family: Eppinga
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  - family: Faul
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  - family: Fisher
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  - family: Forrester
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  - family: Franco
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  - family: Friedlander
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  - family: Ghanbari
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  - family: Giulianini
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  - family: Grabe
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  - family: Grove
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  - family: Gu
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  - family: Harris
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  - family: Heikkinen
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  - family: Heng
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  - family: Hirata
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  - family: Hixson
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  - family: Howard
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  - family: Ikram
    given: M Arfan
  - literal: InterAct Consortium
  - family: Jacobs
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  - family: Johnson
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  - family: Jonas
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  - family: Kammerer
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  - family: Katsuya
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  - family: Khor
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  - family: Kilpeläinen
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  - family: Koh
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  - family: Koistinen
    given: Heikki A
  - family: Kolcic
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  - family: Kooperberg
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  - family: Krieger
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  - family: Kritchevsky
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  - family: Kubo
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  - family: Lakka
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  - family: Langefeld
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  - family: Langenberg
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  - family: Launer
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  - family: Lehne
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  - family: Lemaitre
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  - family: Li
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    given: Tin
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  - family: McKenzie
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  - family: Meitinger
    given: Thomas
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    given: Andres
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  - family: Mosley
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  - family: Nauck
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  - family: Sotoodehnia
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  - family: O'Connell
    given: Jeff R
  - family: Palmer
    given: Nicholette D
  - family: Pazoki
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  - family: Pedersen
    given: Nancy L
  - family: Peters
    given: Annette
  - family: Peyser
    given: Patricia A
  - family: Polasek
    given: Ozren
  - family: Poulter
    given: Neil
  - family: Raffel
    given: Leslie J
  - family: Raitakari
    given: Olli T
  - family: Reiner
    given: Alex P
  - family: Rice
    given: Treva K
  - family: Rich
    given: Stephen S
  - family: Robino
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  - family: Robinson
    given: Jennifer G
  - family: Rose
    given: Lynda M
  - family: Rudan
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  - family: Schmidt
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  - family: Schreiner
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  - family: Scott
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  - family: Sever
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  - family: Shi
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  - family: Sidney
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  - family: Sims
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  - family: Smith
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  - family: Smith
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  - family: Snieder
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  - family: Starr
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  - family: Strauch
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  - family: Tan
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  - family: Taylor
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  - family: Teo
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  - family: Tham
    given: Yih Chung
  - family: Uitterlinden
    given: André G
  - dropping-particle: van
    family: Heemst
    given: Diana
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    given: Dragana
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  - family: Wang
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  - family: Wang
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  - family: Wei
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  - family: Williams
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  - family: Wilson
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  - family: Wojczynski
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  - family: Yao
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  - family: Yu
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  - family: Yu
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  - family: Yuan
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  - family: Becker
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  - family: Esko
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  - family: Farrall
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  - family: Franks
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  - family: Freedman
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  - family: Froguel
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  - family: Gasparini
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  - family: Gieger
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  - family: Horta
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  - family: Kamatani
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  - family: Kato
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  - family: Kooner
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  - family: Laakso
    given: Markku
  - family: Leander
    given: Karin
  - family: Lehtimäki
    given: Terho
  - literal: Lifelines Cohort, Groningen, The Netherlands (Lifelines
      Cohort Study)
  - family: Magnusson
    given: Patrik K E
  - family: Penninx
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  - family: Pereira
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  - family: Rauramaa
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  - family: Wareham
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  - family: Wickremasinghe
    given: Ananda R
  - family: Zheng
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  - family: North
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  - family: Bouchard
    given: Claude
  - family: Evans
    given: Michele K
  - family: Gudnason
    given: Vilmundur
  - family: Liu
    given: Ching-Ti
  - family: Liu
    given: Yongmei
  - family: Psaty
    given: Bruce M
  - family: Ridker
    given: Paul M
  - dropping-particle: van
    family: Dam
    given: Rob M
  - family: Kardia
    given: Sharon L R
  - family: Zhu
    given: Xiaofeng
  - family: Rotimi
    given: Charles N
  - family: Mook-Kanamori
    given: Dennis O
  - family: Fornage
    given: Myriam
  - family: Kelly
    given: Tanika N
  - family: Fox
    given: Ervin R
  - family: Hayward
    given: Caroline
  - dropping-particle: van
    family: Duijn
    given: Cornelia M
  - family: Tai
    given: E Shyong
  - family: Wong
    given: Tien Yin
  - family: Liu
    given: Jingmin
  - family: Rotter
    given: Jerome I
  - family: Gauderman
    given: W James
  - family: Province
    given: Michael A
  - family: Munroe
    given: Patricia B
  - family: Rice
    given: Kenneth
  - family: Chasman
    given: Daniel I
  - family: Cupples
    given: L Adrienne
  - family: Rao
    given: Dabeeru C
  - family: Morrison
    given: Alanna C
  container-title: American Journal of Epidemiology
  doi: 10.1093/aje/kwz005
  id: de_vries_multiancestry_2019
  issn: 0002-9262, 1476-6256
  issue: 6
  issued: 2019-06
  page: 1033-1054
  title: Multiancestry Genome-Wide Association Study of Lipid Levels
    Incorporating Gene-Alcohol Interactions
  type: article-journal
  url: "https://academic.oup.com/aje/article/188/6/1033/5304469"
  volume: 188
  journal-title: '*American Journal of Epidemiology*'
  date: 2019-06
  path: https://doi.org/10.1093/aje/kwz005
  position: '79/256'
  first: '&emsp;&emsp;&emsp;'
- abstract: AbstractMany genetic loci affect circulating lipid levels,
    but it remains unknown whether lifestyle factors, such as physical
    activity, modify these genetic effects. To identify lipid loci
    interacting with physical activity, we performed genome-wide
    analyses of circulating HDL cholesterol, LDL cholesterol, and
    triglyceride levels in up to 120,979 individuals of European,
    African, Asian, Hispanic, and Brazilian ancestry, with follow-up of
    suggestive associations in an additional 131,012 individuals. We
    find four loci, in/near CLASP1 , LHX1 , SNTA1 , and CNTNAP2 , that
    are associated with circulating lipid levels through interaction
    with physical activity; higher levels of physical activity enhance
    the HDL cholesterol-increasing effects of the CLASP1 , LHX1 , and
    SNTA1 loci and attenuate the LDL cholesterol-increasing effect of
    the CNTNAP2 locus. The CLASP1 , LHX1 , and SNTA1 regions harbor
    genes linked to muscle function and lipid metabolism. Our results
    elucidate the role of physical activity interactions in the genetic
    contribution to blood lipid levels.
  accessed: 2023-03-04
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  - family: Bentley
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  - family: Noordam
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  - family: Jakupović
    given: Hermina
  - family: Chasman
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  - family: Manning
    given: Alisa
  - family: Ntalla
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  - family: Aschard
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  - family: Brown
    given: Michael R.
  - dropping-particle: de las
    family: Fuentes
    given: Lisa
  - family: Franceschini
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  - family: Guo
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  - family: Campbell
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  - family: Canouil
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  - family: Chen
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  - family: Concas
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  - family: Connell
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  - dropping-particle: de
    family: Mutsert
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  - family: Kutalik
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  - family: Lewis
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  - family: Liang
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  - literal: Lifelines Cohort Study
  - family: Alizadeh
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  - family: Boezen
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  - family: Franke
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  - family: Navis
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  - dropping-particle: van
    family: Heemst
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  - family: Voortman
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  - family: Waldenberger
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  - family: Wennberg
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  id: kilpelainen_multi-ancestry_2019
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  issue: 11
  issued: 2018-11
  page: 1505-1513
  title: Fine-mapping type 2 diabetes loci to single-variant resolution
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- abstract: Connecting melatonin receptor variants to signaling
    differences reveals paths to type 2 diabetes therapy. , Melatonin
    meets diabetesSome of the single-nucleotide polymorphisms associated
    with type 2 diabetes (T2D) occur in the gene encoding the melatonin
    receptor MT 2 , a G protein--coupled receptor (GPCR). Karamitri et
    al . measured the spontaneous and melatonin-stimulated signaling of
    40 different MT 2 variants. Computational analysis of these
    signaling profiles and assessment of genetic association data showed
    that those MT 2 variants with defective melatonin-stimulated G
    protein signaling and reduced spontaneous β-arrestin recruitment
    were associated with the greatest risk for T2D. These data may aid
    in the development of specific treatments for T2D depending on the
    patient's MT 2 variant. Moreover, the experimental approach may be
    applied to assess the impact of other GPCR mutations on disease
    associations.,Melatonin is produced during the night and regulates
    sleep and circadian rhythms. Loss-of-function variants in MTNR1B ,
    which encodes the melatonin receptor MT 2 , a G protein--coupled
    receptor (GPCR), are associated with an increased risk of type 2
    diabetes (T2D). To identify specific T2D-associated signaling
    pathway(s), we profiled the signaling output of 40 MT 2 variants by
    monitoring spontaneous (ligand-independent) and melatonin-induced
    activation of multiple signaling effectors. Genetic association
    analysis showed that defects in the melatonin-induced activation of
    Gα i1 and Gα z proteins and in spontaneous β-arrestin2 recruitment
    to MT 2 were the most statistically significantly associated with an
    increased T2D risk. Computational variant impact prediction by in
    silico evolutionary lineage analysis strongly correlated with the
    measured phenotypic effect of each variant, providing a predictive
    tool for future studies on GPCR variants. Together, this large-scale
    functional study provides an operational framework for the
    postgenomic analysis of the multiple GPCR variants present in the
    human population. The association of T2D risk with signaling
    pathway--specific defects opens avenues for pathway-specific
    personalized therapeutic intervention and reveals the potential
    relevance of MT 2 function during the day, when melatonin is
    undetectable, but spontaneous activity of the receptor occurs.
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  container-title: Science Signaling
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  id: karamitri_type_2018
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  issued: 2018-08
  page: eaan6622
  title: Type 2 diabetes--associated variants of the MT $_{\textrm{2}}$
    melatonin receptor affect distinct modes of signaling
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  url: "https://www.science.org/doi/10.1126/scisignal.aan6622"
  volume: 11
  journal-title: '*Science Signaling*'
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  - family: Watkins
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  - family: Wu
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  - family: Zheng
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  - family: Bouchard
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  - family: Christensen
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  - family: Evans
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  - family: Gudnason
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    given: L. Adrienne
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  - dropping-particle: van
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  container-title: PLOS ONE
  doi: 10.1371/journal.pone.0198166
  editor:
  - family: Kuivaniemi
    given: Helena
  id: feitosa_novel_2018
  issn: 1932-6203
  issue: 6
  issued: 2018-06
  page: e0198166
  title: Novel genetic associations for blood pressure identified via
    gene-alcohol interaction in up to 570K individuals across multiple
    ancestries
  type: article-journal
  url: "https://dx.plos.org/10.1371/journal.pone.0198166"
  volume: 13
  journal-title: '*PLOS ONE*'
  date: 2018-06
  path: https://doi.org/10.1371/journal.pone.0198166
  position: '86/267'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  annote: first
  author:
  - family: Canouil
    given: Mickaël
  - family: Balkau
    given: Beverley
  - family: Roussel
    given: Ronan
  - family: Froguel
    given: Philippe
  - family: Rocheleau
    given: Ghislain
  container-title: Frontiers in Genetics
  doi: 10.3389/fgene.2018.00210
  id: canouil_jointly_2018
  issn: 1664-8021
  issued: 2018-06
  page: 210
  title: "Jointly Modelling Single Nucleotide Polymorphisms With
    Longitudinal and Time-to-Event Trait: An Application to Type 2
    Diabetes and Fasting Plasma Glucose"
  title-short: Jointly Modelling Single Nucleotide Polymorphisms With
    Longitudinal and Time-to-Event Trait
  type: article-journal
  url: "https://www.frontiersin.org/article/10.3389/fgene.2018.00210/full"
  volume: 9
  journal-title: '*Frontiers in Genetics*'
  date: 2018-06
  path: https://doi.org/10.3389/fgene.2018.00210
  position: '1/5'
  first: '*As first or co-first*'
- abstract: In type 2 diabetes (T2D), hepatic insulin resistance is
    strongly associated with nonalcoholic fatty liver disease (NAFLD).
    In this study, we hypothesized that the DNA methylome of livers from
    patients with T2D compared with livers of individuals with normal
    plasma glucose levels can unveil some mechanism of hepatic insulin
    resistance that could link to NAFLD. Using DNA methylome and
    transcriptome analyses of livers from obese individuals, we found
    that hypomethylation at a CpG site in PDGFA (encoding
    platelet-derived growth factor α) and PDGFA overexpression are both
    associated with increased T2D risk, hyperinsulinemia, increased
    insulin resistance, and increased steatohepatitis risk. Genetic risk
    score studies and human cell modeling pointed to a causative effect
    of high insulin levels on PDGFA CpG site hypomethylation, PDGFA
    overexpression, and increased PDGF-AA secretion from the liver. We
    found that PDGF-AA secretion further stimulates its own expression
    through protein kinase C activity and contributes to insulin
    resistance through decreased expression of insulin receptor
    substrate 1 and of insulin receptor. Importantly, hepatocyte insulin
    sensitivity can be restored by PDGF-AA--blocking antibodies, PDGF
    receptor inhibitors, and by metformin, opening therapeutic avenues.
    Therefore, in the liver of obese patients with T2D, the increased
    PDGF-AA signaling contributes to insulin resistance, opening new
    therapeutic avenues against T2D and possibly NAFLD.
  accessed: 2023-03-04
  annote: first
  author:
  - family: Abderrahmani
    given: Amar
  - family: Yengo
    given: Loïc
  - family: Caiazzo
    given: Robert
  - family: Canouil
    given: Mickaël
  - family: Cauchi
    given: Stéphane
  - family: Raverdy
    given: Violeta
  - family: Plaisance
    given: Valérie
  - family: Pawlowski
    given: Valérie
  - family: Lobbens
    given: Stéphane
  - family: Maillet
    given: Julie
  - family: Rolland
    given: Laure
  - family: Boutry
    given: Raphael
  - family: Queniat
    given: Gurvan
  - family: Kwapich
    given: Maxime
  - family: Tenenbaum
    given: Mathie
  - family: Bricambert
    given: Julien
  - family: Saussenthaler
    given: Sophie
  - family: Anthony
    given: Elodie
  - family: Jha
    given: Pooja
  - family: Derop
    given: Julien
  - family: Sand
    given: Olivier
  - family: Rabearivelo
    given: Iandry
  - family: Leloire
    given: Audrey
  - family: Pigeyre
    given: Marie
  - family: Daujat-Chavanieu
    given: Martine
  - family: Gerbal-Chaloin
    given: Sabine
  - family: Dayeh
    given: Tasnim
  - family: Lassailly
    given: Guillaume
  - family: Mathurin
    given: Philippe
  - family: Staels
    given: Bart
  - family: Auwerx
    given: Johan
  - family: Schürmann
    given: Annette
  - family: Postic
    given: Catherine
  - family: Schafmayer
    given: Clemens
  - family: Hampe
    given: Jochen
  - family: Bonnefond
    given: Amélie
  - family: Pattou
    given: François
  - family: Froguel
    given: Philippe
  container-title: Diabetes
  doi: 10.2337/db17-1539
  id: abderrahmani_increased_2018
  issn: 0012-1797, 1939-327X
  issue: 7
  issued: 2018-07
  page: 1310-1321
  title: Increased Hepatic PDGF-AA Signaling Mediates Liver Insulin
    Resistance in Obesity-Associated Type 2 Diabetes
  type: article-journal
  url: "https://diabetesjournals.org/diabetes/article/67/7/1310/35346/Increased-Hepatic-PDGF-AA-Signaling-Mediates-Liver"
  volume: 67
  journal-title: '*Diabetes*'
  date: 2018-07
  path: https://doi.org/10.2337/db17-1539
  position: '4/38'
  first: '*As first or co-first*'
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  container-title: Nature Genetics
  doi: 10.1038/s41588-018-0084-1
  id: mahajan_refining_2018
  issn: 1061-4036, 1546-1718
  issue: 4
  issued: 2018-04
  page: 559-571
  title: Refining the accuracy of validated target identification
    through coding variant fine-mapping in type 2 diabetes
  type: article-journal
  url: "https://www.nature.com/articles/s41588-018-0084-1"
  volume: 50
  journal-title: '*Nature Genetics*'
  date: 2018-04
  path: https://doi.org/10.1038/s41588-018-0084-1
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    given: Mickaël
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    given: Aravinda
  - family: Chauhan
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    given: John M.
  - dropping-particle: de
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    given: Renée
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  - family: O'Connell
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  - dropping-particle: van
    family: Dam
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  - family: Sims
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  - family: Arnett
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  - family: Mook-Kanamori
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  - family: Kelly
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  - family: Hayward
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  - family: Fornage
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  - family: Rotimi
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  - dropping-particle: van
    family: Duijn
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  - family: Tai
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  - family: Wong
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  - family: Loos
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  - family: Reiner
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  - family: Rotter
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  - family: Zhu
    given: Xiaofeng
  - family: Bierut
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  - family: Gauderman
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  - family: Caulfield
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  - family: Elliott
    given: Paul
  - family: Rice
    given: Kenneth
  - family: Munroe
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  - family: Morrison
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  - family: Cupples
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  - family: Rao
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  - family: Chasman
    given: Daniel I.
  container-title: The American Journal of Human Genetics
  doi: 10.1016/j.ajhg.2018.01.015
  id: sung_large-scale_2018
  issn: 00029297
  issue: 3
  issued: 2018-03
  page: 375-400
  title: A Large-Scale Multi-ancestry Genome-wide Study Accounting for
    Smoking Behavior Identifies Multiple Significant Loci for Blood
    Pressure
  type: article-journal
  url: "https://linkinghub.elsevier.com/retrieve/pii/S000292971830017X"
  volume: 102
  journal-title: '*The American Journal of Human Genetics*'
  date: 2018-03
  path: https://doi.org/10.1016/j.ajhg.2018.01.015
  position: '91/288'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  annote: first
  author:
  - family: Verbanck
    given: Marie
  - family: Canouil
    given: Mickaël
  - family: Leloire
    given: Audrey
  - family: Dhennin
    given: Véronique
  - family: Coumoul
    given: Xavier
  - family: Yengo
    given: Loïc
  - family: Froguel
    given: Philippe
  - family: Poulain-Godefroy
    given: Odile
  container-title: PLOS ONE
  doi: 10.1371/journal.pone.0179583
  editor:
  - family: Guillou
    given: Hervé
  id: verbanck_low-dose_2017
  issn: 1932-6203
  issue: 6
  issued: 2017-06
  page: e0179583
  title: Low-dose exposure to bisphenols A, F and S of human primary
    adipocyte impacts coding and non-coding RNA profiles
  type: article-journal
  url: "https://dx.plos.org/10.1371/journal.pone.0179583"
  volume: 12
  journal-title: '*PLOS ONE*'
  date: 2017-06
  path: https://doi.org/10.1371/journal.pone.0179583
  position: '2/9'
  first: '*As first or co-first*'
- accessed: 2023-03-04
  annote: first
  author:
  - family: Ndiaye
    given: Fatou K.
  - family: Ortalli
    given: Ana
  - family: Canouil
    given: Mickaël
  - family: Huyvaert
    given: Marlène
  - family: Salazar-Cardozo
    given: Clara
  - family: Lecoeur
    given: Cécile
  - family: Verbanck
    given: Marie
  - family: Pawlowski
    given: Valérie
  - family: Boutry
    given: Raphaël
  - family: Durand
    given: Emmanuelle
  - family: Rabearivelo
    given: Iandry
  - family: Sand
    given: Olivier
  - family: Marselli
    given: Lorella
  - family: Kerr-Conte
    given: Julie
  - family: Chandra
    given: Vikash
  - family: Scharfmann
    given: Raphaël
  - family: Poulain-Godefroy
    given: Odile
  - family: Marchetti
    given: Piero
  - family: Pattou
    given: François
  - family: Abderrahmani
    given: Amar
  - family: Froguel
    given: Philippe
  - family: Bonnefond
    given: Amélie
  container-title: Molecular Metabolism
  doi: 10.1016/j.molmet.2017.03.011
  id: ndiaye_expression_2017
  issn: 22128778
  issue: 6
  issued: 2017-06
  page: 459-470
  title: Expression and functional assessment of candidate type 2
    diabetes susceptibility genes identify four new genes contributing
    to human insulin secretion
  type: article-journal
  url: "https://linkinghub.elsevier.com/retrieve/pii/S2212877817301199"
  volume: 6
  journal-title: '*Molecular Metabolism*'
  date: 2017-06
  path: https://doi.org/10.1016/j.molmet.2017.03.011
  position: '3/22'
  first: '*As first or co-first*'
- accessed: 2023-03-04
  author:
  - family: Bonnefond
    given: Amélie
  - family: Yengo
    given: Loïc
  - family: Dechaume
    given: Aurélie
  - family: Canouil
    given: Mickaël
  - family: Castelain
    given: Maxime
  - family: Roger
    given: Estelle
  - family: Allegaert
    given: Frédéric
  - family: Caiazzo
    given: Robert
  - family: Raverdy
    given: Violeta
  - family: Pigeyre
    given: Marie
  - family: Arredouani
    given: Abdelilah
  - family: Borys
    given: Jean-Michel
  - family: Lévy-Marchal
    given: Claire
  - family: Weill
    given: Jacques
  - family: Roussel
    given: Ronan
  - family: Balkau
    given: Beverley
  - family: Marre
    given: Michel
  - family: Pattou
    given: François
  - family: Brousseau
    given: Thierry
  - family: Froguel
    given: Philippe
  container-title: BMC Medicine
  doi: 10.1186/s12916-017-0784-x
  id: bonnefond_relationship_2017
  issn: 1741-7015
  issue: 1
  issued: 2017-12
  page: 37
  title: "Relationship between salivary/pancreatic amylase and body mass
    index: A systems biology approach"
  title-short: Relationship between salivary/pancreatic amylase and body
    mass index
  type: article-journal
  url: "http://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-017-0784-x"
  volume: 15
  journal-title: '*BMC Medicine*'
  date: 2017-12
  path: https://doi.org/10.1186/s12916-017-0784-x
  position: '4/20'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - family: Carrat
    given: Gaelle R.
  - family: Hu
    given: Ming
  - family: Nguyen-Tu
    given: Marie-Sophie
  - family: Chabosseau
    given: Pauline
  - family: Gaulton
    given: Kyle J.
  - dropping-particle: van de
    family: Bunt
    given: Martijn
  - family: Siddiq
    given: Afshan
  - family: Falchi
    given: Mario
  - family: Thurner
    given: Matthias
  - family: Canouil
    given: Mickaël
  - family: Pattou
    given: Francois
  - family: Leclerc
    given: Isabelle
  - family: Pullen
    given: Timothy J.
  - family: Cane
    given: Matthew C.
  - family: Prabhala
    given: Priyanka
  - family: Greenwald
    given: William
  - family: Schulte
    given: Anke
  - family: Marchetti
    given: Piero
  - family: Ibberson
    given: Mark
  - family: MacDonald
    given: Patrick E.
  - family: Manning Fox
    given: Jocelyn E.
  - family: Gloyn
    given: Anna L.
  - family: Froguel
    given: Philippe
  - family: Solimena
    given: Michele
  - family: McCarthy
    given: Mark I.
  - family: Rutter
    given: Guy A.
  container-title: The American Journal of Human Genetics
  doi: 10.1016/j.ajhg.2017.01.011
  id: carrat_decreased_2017
  issn: 00029297
  issue: 2
  issued: 2017-02
  page: 238-256
  title: Decreased STARD10 Expression Is Associated with Defective
    Insulin Secretion in Humans and Mice
  type: article-journal
  url: "https://linkinghub.elsevier.com/retrieve/pii/S0002929717300113"
  volume: 100
  journal-title: '*The American Journal of Human Genetics*'
  date: 2017-02
  path: https://doi.org/10.1016/j.ajhg.2017.01.011
  position: '9/25'
  first: '&emsp;&emsp;&emsp;'
- abstract: Hepatic DPP4 expression is elevated in subjects with ectopic
    fat accumulation in the liver. However, whether increased dipeptidyl
    peptidase 4 (DPP4) is involved in the pathogenesis or is rather a
    consequence of metabolic disease is not known. We therefore studied
    the transcriptional regulation of hepatic Dpp4 in young mice prone
    to diet-induced obesity. Already at 6 weeks of age, expression of
    hepatic Dpp4 was increased in mice with high weight gain,
    independent of liver fat content. In the same animals, methylation
    of four intronic CpG sites was decreased, amplifying glucose-induced
    transcription of hepatic Dpp4. In older mice, hepatic triglyceride
    content was increased only in animals with elevated Dpp4 expression.
    Expression and release of DPP4 were markedly higher in the liver
    compared with adipose depots. Analysis of human liver biopsy
    specimens revealed a correlation of DPP4 expression and DNA
    methylation to stages of hepatosteatosis and nonalcoholic
    steatohepatitis. In summary, our results indicate a crucial role of
    the liver in participation to systemic DPP4 levels. Furthermore, the
    data show that glucose-induced expression of Dpp4 in the liver is
    facilitated by demethylation of the Dpp4 gene early in life. This
    might contribute to early deteriorations in hepatic function, which
    in turn result in metabolic disease such as hepatosteatosis later in
    life.
  accessed: 2023-03-04
  author:
  - family: Baumeier
    given: Christian
  - family: Saussenthaler
    given: Sophie
  - family: Kammel
    given: Anne
  - family: Jähnert
    given: Markus
  - family: Schlüter
    given: Luisa
  - family: Hesse
    given: Deike
  - family: Canouil
    given: Mickaël
  - family: Lobbens
    given: Stephane
  - family: Caiazzo
    given: Robert
  - family: Raverdy
    given: Violeta
  - family: Pattou
    given: François
  - family: Nilsson
    given: Emma
  - family: Pihlajamäki
    given: Jussi
  - family: Ling
    given: Charlotte
  - family: Froguel
    given: Philippe
  - family: Schürmann
    given: Annette
  - family: Schwenk
    given: Robert W.
  container-title: Diabetes
  doi: 10.2337/db15-1716
  id: baumeier_hepatic_2017
  issn: 0012-1797, 1939-327X
  issue: 1
  issued: 2017-01
  page: 25-35
  title: Hepatic *DPP4* DNA Methylation Associates With Fatty Liver
  type: article-journal
  url: "https://diabetesjournals.org/diabetes/article/66/1/25/40137/Hepatic-DPP4-DNA-Methylation-Associates-With-Fatty"
  volume: 66
  journal-title: '*Diabetes*'
  date: 2017-01
  path: https://doi.org/10.2337/db15-1716
  position: '7/17'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - family: Yengo
    given: Loïc
  - family: Jacques
    given: Julien
  - family: Biernacki
    given: Christophe
  - family: Canouil
    given: Mickael
  container-title: The R Journal
  doi: 10.32614/RJ-2016-006
  id: yengo_variable_2016
  issn: 2073-4859
  issue: 1
  issued: 2016-04
  page: 92
  title: "Variable Clustering in High-Dimensional Linear Regression: The
    R Package clere"
  title-short: Variable Clustering in High-Dimensional Linear Regression
  type: article-journal
  url: "https://journal.r-project.org/archive/2016/RJ-2016-006/index.html"
  volume: 8
  journal-title: '*The R Journal*'
  date: 2016-04
  path: https://doi.org/10.32614/RJ-2016-006
  position: '4/4'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2023-03-04
  author:
  - family: Folon
    given: Lise
  - family: Baron
    given: Morgane
  - family: Toussaint
    given: Bénédicte
  - family: Vaillant
    given: Emmanuel
  - family: Boissel
    given: Mathilde
  - family: Scherrer
    given: Victoria
  - family: Loiselle
    given: Hélène
  - family: Leloire
    given: Audrey
  - family: Badreddine
    given: Alaa
  - family: Balkau
    given: Beverley
  - family: Charpentier
    given: Guillaume
  - family: Franc
    given: Sylvia
  - family: Marre
    given: Michel
  - family: Aboulouard
    given: Soulaimane
  - family: Salzet
    given: Michel
  - family: Canouil
    given: Mickaël
  - family: Derhourhi
    given: Mehdi
  - family: Froguel
    given: Philippe
  - family: Bonnefond
    given: Amélie
  container-title: The Lancet Diabetes & Endocrinology
  doi: 10.1016/S2213-8587(22)00392-8
  id: folon_contribution_2023
  issn: 22138587
  issue: 3
  issued: 2023-03
  page: 182-190
  title: "Contribution of heterozygous PCSK1 variants to obesity and
    implications for precision medicine: A case-control study"
  title-short: Contribution of heterozygous PCSK1 variants to obesity
    and implications for precision medicine
  type: article-journal
  url: "https://linkinghub.elsevier.com/retrieve/pii/S2213858722003928"
  volume: 11
  journal-title: '*The Lancet Diabetes & Endocrinology*'
  date: 2023-03
  path: https://doi.org/10.1016/S2213-8587(22)00392-8
  position: '16/19'
  first: '&emsp;&emsp;&emsp;'
- abstract: Chronic kidney disease (CKD) is responsible for a public
    health burden with multi-systemic complications. Through
    trans-ancestry meta-analysis of genome-wide association studies of
    estimated glomerular filtration rate (eGFR) and independent
    replication (n = 1,046,070), we identified 264 associated loci (166
    new). Of these, 147 were likely to be relevant for kidney function
    on the basis of associations with the alternative kidney function
    marker blood urea nitrogen (n = 416,178). Pathway and enrichment
    analyses, including mouse models with renal phenotypes, support the
    kidney as the main target organ. A genetic risk score for lower eGFR
    was associated with clinically diagnosed CKD in 452,264 independent
    individuals. Colocalization analyses of associations with eGFR among
    783,978 European-ancestry individuals and gene expression across 46
    human tissues, including tubulo-interstitial and glomerular kidney
    compartments, identified 17 genes differentially expressed in
    kidney. Fine-mapping highlighted missense driver variants in 11
    genes and kidney-specific regulatory variants. These results provide
    a comprehensive priority list of molecular targets for translational
    research.
  author:
  - family: Wuttke
    given: Matthias
  - family: Li
    given: Yong
  - family: Li
    given: Man
  - family: Sieber
    given: Karsten B.
  - family: Feitosa
    given: Mary F.
  - family: Gorski
    given: Mathias
  - family: Tin
    given: Adrienne
  - family: Wang
    given: Lihua
  - family: Chu
    given: Audrey Y.
  - family: Hoppmann
    given: Anselm
  - family: Kirsten
    given: Holger
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  - family: Perola
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  - family: Pirastu
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  - family: Pistis
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  - family: Tzoulaki
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  - family: Vaccargiu
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    family: Dam
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    family: Harst
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    family: Duijn
    given: Cornelia M.
  - family: Velez Edward
    given: Digna R.
  - family: Verweij
    given: Niek
  - family: Vogelezang
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    given: Uwe
  - family: Vollenweider
    given: Peter
  - family: Waeber
    given: Gerard
  - family: Waldenberger
    given: Melanie
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    given: Qiong
  - literal: Lifelines Cohort Study
  - literal: V. A. Million Veteran Program
  container-title: Nature Genetics
  doi: 10.1038/s41588-019-0407-x
  id: wuttke_catalog_2019
  issn: 1546-1718
  issue: 6
  issued: 2019-06
  page: 957-972
  title: A catalog of genetic loci associated with kidney function from
    analyses of a million individuals
  type: article-journal
  url: "https://doi.org/10.1038/s41588-019-0407-x"
  volume: 51
  journal-title: '*Nature Genetics*'
  date: 2019-06
  path: https://doi.org/10.1038/s41588-019-0407-x
  position: '50/291'
  first: '&emsp;&emsp;&emsp;'
- abstract: "Abstract We identify biomarkers for disease progression in
    three type 2 diabetes cohorts encompassing 2,973 individuals across
    three molecular classes, metabolites, lipids and proteins.
    Homocitrulline, isoleucine and 2-aminoadipic acid, eight
    triacylglycerol species, and lowered sphingomyelin 42:2;2 levels are
    predictive of faster progression towards insulin requirement. Of
    \\~1,300 proteins examined in two cohorts, levels of GDF15/MIC-1,
    IL-18Ra, CRELD1, NogoR, FAS, and ENPP7 are associated with faster
    progression, whilst SMAC/DIABLO, SPOCK1 and HEMK2 predict lower
    progression rates. In an external replication, proteins and lipids
    are associated with diabetes incidence and prevalence. NogoR/RTN4R
    injection improved glucose tolerance in high fat-fed male mice but
    impaired it in male db/db mice. High NogoR levels led to islet cell
    apoptosis, and IL-18R antagonised inflammatory IL-18 signalling
    towards nuclear factor kappa-B in vitro. This comprehensive,
    multi-disciplinary approach thus identifies biomarkers with
    potential prognostic utility, provides evidence for possible disease
    mechanisms, and identifies potential therapeutic avenues to slow
    diabetes progression."
  accessed: 2023-05-12
  author:
  - family: Slieker
    given: Roderick C.
  - family: Donnelly
    given: Louise A.
  - family: Akalestou
    given: Elina
  - family: Lopez-Noriega
    given: Livia
  - family: Melhem
    given: Rana
  - family: Güneş
    given: Ayşim
  - family: Abou Azar
    given: Frederic
  - family: Efanov
    given: Alexander
  - family: Georgiadou
    given: Eleni
  - family: Muniangi-Muhitu
    given: Hermine
  - family: Sheikh
    given: Mahsa
  - family: Giordano
    given: Giuseppe N.
  - family: Åkerlund
    given: Mikael
  - family: Ahlqvist
    given: Emma
  - family: Ali
    given: Ashfaq
  - family: Banasik
    given: Karina
  - family: Brunak
    given: Søren
  - family: Barovic
    given: Marko
  - family: Bouland
    given: Gerard A.
  - family: Burdet
    given: Frédéric
  - family: Canouil
    given: Mickaël
  - family: Dragan
    given: Iulian
  - family: Elders
    given: Petra J. M.
  - family: Fernandez
    given: Celine
  - family: Festa
    given: Andreas
  - family: Fitipaldi
    given: Hugo
  - family: Froguel
    given: Phillippe
  - family: Gudmundsdottir
    given: Valborg
  - family: Gudnason
    given: Vilmundur
  - family: Gerl
    given: Mathias J.
  - dropping-particle: van der
    family: Heijden
    given: Amber A.
  - family: Jennings
    given: Lori L.
  - family: Hansen
    given: Michael K.
  - family: Kim
    given: Min
  - family: Leclerc
    given: Isabelle
  - family: Klose
    given: Christian
  - family: Kuznetsov
    given: Dmitry
  - family: Mansour Aly
    given: Dina
  - family: Mehl
    given: Florence
  - family: Marek
    given: Diana
  - family: Melander
    given: Olle
  - family: Niknejad
    given: Anne
  - family: Ottosson
    given: Filip
  - family: Pavo
    given: Imre
  - family: Duffin
    given: Kevin
  - family: Syed
    given: Samreen K.
  - family: Shaw
    given: Janice L.
  - family: Cabrera
    given: Over
  - family: Pullen
    given: Timothy J.
  - family: Simons
    given: Kai
  - family: Solimena
    given: Michele
  - family: Suvitaival
    given: Tommi
  - family: Wretlind
    given: Asger
  - family: Rossing
    given: Peter
  - family: Lyssenko
    given: Valeriya
  - family: Legido Quigley
    given: Cristina
  - family: Groop
    given: Leif
  - family: Thorens
    given: Bernard
  - family: Franks
    given: Paul W.
  - family: Lim
    given: Gareth E.
  - family: Estall
    given: Jennifer
  - family: Ibberson
    given: Mark
  - family: Beulens
    given: Joline W. J.
  - dropping-particle: "'t"
    family: Hart
    given: Leen M
  - family: Pearson
    given: Ewan R.
  - family: Rutter
    given: Guy A.
  container-title: Nature Communications
  doi: 10.1038/s41467-023-38148-7
  id: slieker_identification_2023
  issn: 2041-1723
  issue: 1
  issued: 2023-05
  page: 2533
  title: Identification of biomarkers for glycaemic deterioration in
    type 2 diabetes
  type: article-journal
  url: "https://www.nature.com/articles/s41467-023-38148-7"
  volume: 14
  journal-title: '*Nature Communications*'
  date: 2023-05
  path: https://doi.org/10.1038/s41467-023-38148-7
  position: '21/64'
  first: '&emsp;&emsp;&emsp;'
- abstract: "AbstractImportance and Objective The identification of
    myokines susceptible to improve glucose homeostasis following
    bariatric surgery could lead to new therapeutic approaches for type
    2 diabetes.Methods Changes in the homeostasis model assessment
    (HOMA) test were assessed in patients before and 3 months after
    bariatric surgery. Changes in myokines expression and circulating
    levels were assessed using real-time quantitative polymerase chain
    reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA).
    Myokines known to regulate glucose homeostasis were identified using
    literature (targeted study) and putative myokines using
    RNA-sequencing (untargeted study). A linear regression analysis
    adjusted for age and sex was used to search for associations between
    changes in the HOMA test and changes in myokines.Results In the
    targeted study, brain-derived neurotrophic factor (BDNF) expression
    was upregulated (+30%, P = .006) while BDNF circulating levels were
    decreased (−12%, P = .001). Upregulated BDNF expression was
    associated with decreased HOMA of insulin resistance (HOMA-IR)
    (adjusted estimate \\[95% confidence interval {CI}\\]: −0.51 \\[−0.88
    to −0.13\\], P = .010). Decreased BDNF serum levels were associated
    with decreased HOMA of beta-cell function (HOMA-B) (adjusted
    estimate \\[95% CI\\] = 0.002 \\[0.00002-0.0031\\], P = .046). In the
    untargeted study, upregulated putative myokines included XYLT1
    (+64%, P &lt; .001), LGR5 (+57, P&lt; .001), and SPINK5 (+46%, P
    &lt; .001). Upregulated LGR5 was associated with decreased HOMA-IR
    (adjusted estimate \\[95% CI\\] = −0.50 \\[−0.86 to −0.13\\], P = .009).
    Upregulated XYLT1 and SPINK5 were associated with increased HOMA of
    insulin sensitivity (HOMA-S) (respectively, adjusted estimate \\[95%
    CI\\] = 109.1 \\[28.5-189.8\\], P = .009 and 16.5 \\[0.87-32.19\\], P =
    .039).Conclusions Improved glucose homeostasis following bariatric
    surgery is associated with changes in myokines expression and
    circulating levels. In particular, upregulation of BDNF, XYLT1,
    SPINK5, and LGR5 is associated with improved insulin sensitivity.
    These results suggest that these myokines could contribute to
    improved glucose homeostasis following bariatric surgery.Study
    registration NCT03341793 on ClinicalTrials.gov
    (https://clinicaltrials.gov/)."
  accessed: 2023-10-22
  author:
  - family: Orioli
    given: Laura
  - family: Canouil
    given: Mickaël
  - family: Sawadogo
    given: Kiswendsida
  - family: Ning
    given: Lijiao
  - family: Deldicque
    given: Louise
  - family: Lause
    given: Pascale
  - dropping-particle: de
    family: Barsy
    given: Marie
  - family: Froguel
    given: Philippe
  - family: Loumaye
    given: Audrey
  - family: Deswysen
    given: Yannick
  - family: Navez
    given: Benoit
  - family: Bonnefond
    given: Amélie
  - family: Thissen
    given: Jean-Paul
  container-title: European Journal of Endocrinology
  doi: 10.1093/ejendo/lvad122
  id: orioli_identification_2023
  issn: 0804-4643, 1479-683X
  issue: 3
  issued: 2023-09
  page: 409-421
  title: Identification of myokines susceptible to improve glucose
    homeostasis after bariatric surgery
  type: article-journal
  url: "https://academic.oup.com/ejendo/article/189/3/409/7252679"
  volume: 189
  journal-title: '*European Journal of Endocrinology*'
  date: 2023-09
  path: https://doi.org/10.1093/ejendo/lvad122
  position: '2/12'
  first: '&emsp;&emsp;&emsp;'
- accessed: 2024-08-11
  author:
  - family: Meulebrouck
    given: Sarah
  - family: Merrheim
    given: Judith
  - family: Queniat
    given: Gurvan
  - family: Bourouh
    given: Cyril
  - family: Derhourhi
    given: Mehdi
  - family: Boissel
    given: Mathilde
  - family: Yi
    given: Xiaoyan
  - family: Badreddine
    given: Alaa
  - family: Boutry
    given: Raphaël
  - family: Leloire
    given: Audrey
  - family: Toussaint
    given: Bénédicte
  - family: Amanzougarene
    given: Souhila
  - family: Vaillant
    given: Emmanuel
  - family: Durand
    given: Emmanuelle
  - family: Loiselle
    given: Hélène
  - family: Huyvaert
    given: Marlène
  - family: Dechaume
    given: Aurélie
  - family: Scherrer
    given: Victoria
  - family: Marchetti
    given: Piero
  - family: Balkau
    given: Beverley
  - family: Charpentier
    given: Guillaume
  - family: Franc
    given: Sylvia
  - family: Marre
    given: Michel
  - family: Roussel
    given: Ronan
  - family: Scharfmann
    given: Raphaël
  - family: Cnop
    given: Miriam
  - family: Canouil
    given: Mickaël
  - family: Baron
    given: Morgane
  - family: Froguel
    given: Philippe
  - family: Bonnefond
    given: Amélie
  container-title: Nature Communications
  doi: 10.1038/s41467-024-51004-6
  id: meulebrouck_functional_2024
  issn: 2041-1723
  issue: 1
  issued: 2024-08
  page: 6627
  title: Functional genetics reveals the contribution of delta opioid
    receptor to type 2 diabetes and beta-cell function
  type: article-journal
  url: "https://www.nature.com/articles/s41467-024-51004-6"
  volume: 15
  journal-title: '*Nature Communications*'
  date: 2024-08
  path: https://doi.org/10.1038/s41467-024-51004-6
  position: '27/30'
  first: '&emsp;&emsp;&emsp;'
- abstract: AbstractType 2 diabetes (T2D) is a heterogeneous disease
    that develops through diverse pathophysiological processes 1,2 and
    molecular mechanisms that are often specific to cell type 3,4 .
    Here, to characterize the genetic contribution to these processes
    across ancestry groups, we aggregate genome-wide association study
    data from 2,535,601 individuals (39.7% not of European ancestry),
    including 428,452 cases of T2D. We identify 1,289 independent
    association signals at genome-wide significance ( P  \<\< 5 × 10 −8
    ) that map to 611 loci, of which 145 loci are, to our knowledge,
    previously unreported. We define eight non-overlapping clusters of
    T2D signals that are characterized by distinct profiles of
    cardiometabolic trait associations. These clusters are
    differentially enriched for cell-type-specific regions of open
    chromatin, including pancreatic islets, adipocytes, endothelial
    cells and enteroendocrine cells. We build cluster-specific
    partitioned polygenic scores 5 in a further 279,552 individuals of
    diverse ancestry, including 30,288 cases of T2D, and test their
    association with T2D-related vascular outcomes. Cluster-specific
    partitioned polygenic scores are associated with coronary artery
    disease, peripheral artery disease and end-stage diabetic
    nephropathy across ancestry groups, highlighting the importance of
    obesity-related processes in the development of vascular outcomes.
    Our findings show the value of integrating multi-ancestry
    genome-wide association study data with single-cell epigenomics to
    disentangle the aetiological heterogeneity that drives the
    development and progression of T2D. This might offer a route to
    optimize global access to genetically informed diabetes care.
  accessed: 2024-08-11
  author:
  - family: Suzuki
    given: Ken
  - family: Hatzikotoulas
    given: Konstantinos
  - family: Southam
    given: Lorraine
  - family: Taylor
    given: Henry J.
  - family: Yin
    given: Xianyong
  - family: Lorenz
    given: Kim M.
  - family: Mandla
    given: Ravi
  - family: Huerta-Chagoya
    given: Alicia
  - family: Melloni
    given: Giorgio E. M.
  - family: Kanoni
    given: Stavroula
  - family: Rayner
    given: Nigel W.
  - family: Bocher
    given: Ozvan
  - family: Arruda
    given: Ana Luiza
  - family: Sonehara
    given: Kyuto
  - family: Namba
    given: Shinichi
  - family: Lee
    given: Simon S. K.
  - family: Preuss
    given: Michael H.
  - family: Petty
    given: Lauren E.
  - family: Schroeder
    given: Philip
  - family: Vanderwerff
    given: Brett
  - family: Kals
    given: Mart
  - family: Bragg
    given: Fiona
  - family: Lin
    given: Kuang
  - family: Guo
    given: Xiuqing
  - family: Zhang
    given: Weihua
  - family: Yao
    given: Jie
  - family: Kim
    given: Young Jin
  - family: Graff
    given: Mariaelisa
  - family: Takeuchi
    given: Fumihiko
  - family: Nano
    given: Jana
  - family: Lamri
    given: Amel
  - family: Nakatochi
    given: Masahiro
  - family: Moon
    given: Sanghoon
  - family: Scott
    given: Robert A.
  - family: Cook
    given: James P.
  - family: Lee
    given: Jung-Jin
  - family: Pan
    given: Ian
  - family: Taliun
    given: Daniel
  - family: Parra
    given: Esteban J.
  - family: Chai
    given: Jin-Fang
  - family: Bielak
    given: Lawrence F.
  - family: Tabara
    given: Yasuharu
  - family: Hai
    given: Yang
  - family: Thorleifsson
    given: Gudmar
  - family: Grarup
    given: Niels
  - family: Sofer
    given: Tamar
  - family: Wuttke
    given: Matthias
  - family: Sarnowski
    given: Chloé
  - family: Gieger
    given: Christian
  - family: Nousome
    given: Darryl
  - family: Trompet
    given: Stella
  - family: Kwak
    given: Soo-Heon
  - family: Long
    given: Jirong
  - family: Sun
    given: Meng
  - family: Tong
    given: Lin
  - family: Chen
    given: Wei-Min
  - family: Nongmaithem
    given: Suraj S.
  - family: Noordam
    given: Raymond
  - family: Lim
    given: Victor J. Y.
  - family: Tam
    given: Claudia H. T.
  - family: Joo
    given: Yoonjung Yoonie
  - family: Chen
    given: Chien-Hsiun
  - family: Raffield
    given: Laura M.
  - family: Prins
    given: Bram Peter
  - family: Nicolas
    given: Aude
  - family: Yanek
    given: Lisa R.
  - family: Chen
    given: Guanjie
  - family: Brody
    given: Jennifer A.
  - family: Kabagambe
    given: Edmond
  - family: An
    given: Ping
  - family: Xiang
    given: Anny H.
  - family: Choi
    given: Hyeok Sun
  - family: Cade
    given: Brian E.
  - family: Tan
    given: Jingyi
  - family: Broadaway
    given: K. Alaine
  - family: Williamson
    given: Alice
  - family: Kamali
    given: Zoha
  - family: Cui
    given: Jinrui
  - family: Thangam
    given: Manonanthini
  - family: Adair
    given: Linda S.
  - family: Adeyemo
    given: Adebowale
  - family: Aguilar-Salinas
    given: Carlos A.
  - family: Ahluwalia
    given: Tarunveer S.
  - family: Anand
    given: Sonia S.
  - family: Bertoni
    given: Alain
  - family: Bork-Jensen
    given: Jette
  - family: Brandslund
    given: Ivan
  - family: Buchanan
    given: Thomas A.
  - family: Burant
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  - family: Butterworth
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  - family: Canouil
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  - family: Chan
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  - family: Chang
    given: Li-Ching
  - family: Chee
    given: Miao-Li
  - family: Chen
    given: Ji
  - family: Chen
    given: Shyh-Huei
  - family: Chen
    given: Yuan-Tsong
  - family: Chen
    given: Zhengming
  - family: Chuang
    given: Lee-Ming
  - family: Cushman
    given: Mary
  - family: Danesh
    given: John
  - family: Das
    given: Swapan K.
  - family: De Silva
    given: H. Janaka
  - family: Dedoussis
    given: George
  - family: Dimitrov
    given: Latchezar
  - family: Doumatey
    given: Ayo P.
  - family: Du
    given: Shufa
  - family: Duan
    given: Qing
  - family: Eckardt
    given: Kai-Uwe
  - family: Emery
    given: Leslie S.
  - family: Evans
    given: Daniel S.
  - family: Evans
    given: Michele K.
  - family: Fischer
    given: Krista
  - family: Floyd
    given: James S.
  - family: Ford
    given: Ian
  - family: Franco
    given: Oscar H.
  - family: Frayling
    given: Timothy M.
  - family: Freedman
    given: Barry I.
  - family: Genter
    given: Pauline
  - family: Gerstein
    given: Hertzel C.
  - family: Giedraitis
    given: Vilmantas
  - family: González-Villalpando
    given: Clicerio
  - family: González-Villalpando
    given: Maria Elena
  - family: Gordon-Larsen
    given: Penny
  - family: Gross
    given: Myron
  - family: Guare
    given: Lindsay A.
  - family: Hackinger
    given: Sophie
  - family: Hakaste
    given: Liisa
  - family: Han
    given: Sohee
  - family: Hattersley
    given: Andrew T.
  - family: Herder
    given: Christian
  - family: Horikoshi
    given: Momoko
  - family: Howard
    given: Annie-Green
  - family: Hsueh
    given: Willa
  - family: Huang
    given: Mengna
  - family: Huang
    given: Wei
  - family: Hung
    given: Yi-Jen
  - family: Hwang
    given: Mi Yeong
  - family: Hwu
    given: Chii-Min
  - family: Ichihara
    given: Sahoko
  - family: Ikram
    given: Mohammad Arfan
  - family: Ingelsson
    given: Martin
  - family: Islam
    given: Md. Tariqul
  - family: Isono
    given: Masato
  - family: Jang
    given: Hye-Mi
  - family: Jasmine
    given: Farzana
  - family: Jiang
    given: Guozhi
  - family: Jonas
    given: Jost B.
  - family: Jørgensen
    given: Torben
  - family: Kamanu
    given: Frederick K.
  - family: Kandeel
    given: Fouad R.
  - family: Kasturiratne
    given: Anuradhani
  - family: Katsuya
    given: Tomohiro
  - family: Kaur
    given: Varinderpal
  - family: Kawaguchi
    given: Takahisa
  - family: Keaton
    given: Jacob M.
  - family: Kho
    given: Abel N.
  - family: Khor
    given: Chiea-Chuen
  - family: Kibriya
    given: Muhammad G.
  - family: Kim
    given: Duk-Hwan
  - family: Kronenberg
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  - family: Kuusisto
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  - family: Läll
    given: Kristi
  - family: Lange
    given: Leslie A.
  - family: Lee
    given: Kyung Min
  - family: Lee
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  - family: Lee
    given: Nanette R.
  - family: Leong
    given: Aaron
  - family: Li
    given: Liming
  - family: Li
    given: Yun
  - family: Li-Gao
    given: Ruifang
  - family: Ligthart
    given: Symen
  - family: Lindgren
    given: Cecilia M.
  - family: Linneberg
    given: Allan
  - family: Liu
    given: Ching-Ti
  - family: Liu
    given: Jianjun
  - family: Locke
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  - family: Louie
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  - family: Luan
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  - family: Luk
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  - family: Luo
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  - family: Lv
    given: Jun
  - family: Lynch
    given: Julie A.
  - family: Lyssenko
    given: Valeriya
  - family: Maeda
    given: Shiro
  - family: Mamakou
    given: Vasiliki
  - family: Mansuri
    given: Sohail Rafik
  - family: Matsuda
    given: Koichi
  - family: Meitinger
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  - family: Melander
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  - family: Metspalu
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  - family: Mo
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  - family: Moura
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  - family: Nadler
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  - family: Nalls
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  - family: Nayak
    given: Uma
  - family: Ntalla
    given: Ioanna
  - family: Okada
    given: Yukinori
  - family: Orozco
    given: Lorena
  - family: Patel
    given: Sanjay R.
  - family: Patil
    given: Snehal
  - family: Pei
    given: Pei
  - family: Pereira
    given: Mark A.
  - family: Peters
    given: Annette
  - family: Pirie
    given: Fraser J.
  - family: Polikowsky
    given: Hannah G.
  - family: Porneala
    given: Bianca
  - family: Prasad
    given: Gauri
  - family: Rasmussen-Torvik
    given: Laura J.
  - family: Reiner
    given: Alexander P.
  - family: Roden
    given: Michael
  - family: Rohde
    given: Rebecca
  - family: Roll
    given: Katheryn
  - family: Sabanayagam
    given: Charumathi
  - family: Sandow
    given: Kevin
  - family: Sankareswaran
    given: Alagu
  - family: Sattar
    given: Naveed
  - family: Schönherr
    given: Sebastian
  - family: Shahriar
    given: Mohammad
  - family: Shen
    given: Botong
  - family: Shi
    given: Jinxiu
  - family: Shin
    given: Dong Mun
  - family: Shojima
    given: Nobuhiro
  - family: Smith
    given: Jennifer A.
  - family: So
    given: Wing Yee
  - family: Stančáková
    given: Alena
  - family: Steinthorsdottir
    given: Valgerdur
  - family: Stilp
    given: Adrienne M.
  - family: Strauch
    given: Konstantin
  - family: Taylor
    given: Kent D.
  - family: Thorand
    given: Barbara
  - family: Thorsteinsdottir
    given: Unnur
  - family: Tomlinson
    given: Brian
  - family: Tran
    given: Tam C.
  - family: Tsai
    given: Fuu-Jen
  - family: Tuomilehto
    given: Jaakko
  - family: Tusie-Luna
    given: Teresa
  - family: Udler
    given: Miriam S.
  - family: Valladares-Salgado
    given: Adan
  - family: Van Dam
    given: Rob M.
  - family: Van Klinken
    given: Jan B.
  - family: Varma
    given: Rohit
  - family: Wacher-Rodarte
    given: Niels
  - family: Wheeler
    given: Eleanor
  - family: Wickremasinghe
    given: Ananda R.
  - family: Van Dijk
    given: Ko Willems
  - family: Witte
    given: Daniel R.
  - family: Yajnik
    given: Chittaranjan S.
  - family: Yamamoto
    given: Ken
  - family: Yamamoto
    given: Kenichi
  - family: Yoon
    given: Kyungheon
  - family: Yu
    given: Canqing
  - family: Yuan
    given: Jian-Min
  - family: Yusuf
    given: Salim
  - family: Zawistowski
    given: Matthew
  - family: Zhang
    given: Liang
  - family: Zheng
    given: Wei
  - literal: VA Million Veteran Program
  - literal: AMED GRIFIN Diabetes Initiative Japan
  - literal: Biobank Japan Project
  - literal: Penn Medicine BioBank
  - literal: Regeneron Genetics Center
  - literal: Genes & Health Research Team
  - family: Kanona
    given: Stavroula
  - family: Van Heel
    given: David A.
  - literal: eMERGE Consortium
  - literal: International Consortium of Blood Pressure (ICBP)
  - literal: Meta-Analyses of Glucose and Insulin-Related Traits
      Consortium (MAGIC)
  - family: Raffel
    given: Leslie J.
  - family: Igase
    given: Michiya
  - family: Ipp
    given: Eli
  - family: Redline
    given: Susan
  - family: Cho
    given: Yoon Shin
  - family: Lind
    given: Lars
  - family: Province
    given: Michael A.
  - family: Fornage
    given: Myriam
  - family: Hanis
    given: Craig L.
  - family: Ingelsson
    given: Erik
  - family: Zonderman
    given: Alan B.
  - family: Psaty
    given: Bruce M.
  - family: Wang
    given: Ya-Xing
  - family: Rotimi
    given: Charles N.
  - family: Becker
    given: Diane M.
  - family: Matsuda
    given: Fumihiko
  - family: Liu
    given: Yongmei
  - family: Yokota
    given: Mitsuhiro
  - family: Kardia
    given: Sharon L. R.
  - family: Peyser
    given: Patricia A.
  - family: Pankow
    given: James S.
  - family: Engert
    given: James C.
  - family: Bonnefond
    given: Amélie
  - family: Froguel
    given: Philippe
  - family: Wilson
    given: James G.
  - family: Sheu
    given: Wayne H. H.
  - family: Wu
    given: Jer-Yuarn
  - family: Hayes
    given: M. Geoffrey
  - family: Ma
    given: Ronald C. W.
  - family: Wong
    given: Tien-Yin
  - family: Mook-Kanamori
    given: Dennis O.
  - family: Tuomi
    given: Tiinamaija
  - family: Chandak
    given: Giriraj R.
  - family: Collins
    given: Francis S.
  - family: Bharadwaj
    given: Dwaipayan
  - family: Paré
    given: Guillaume
  - family: Sale
    given: Michèle M.
  - family: Ahsan
    given: Habibul
  - family: Motala
    given: Ayesha A.
  - family: Shu
    given: Xiao-Ou
  - family: Park
    given: Kyong-Soo
  - family: Jukema
    given: J. Wouter
  - family: Cruz
    given: Miguel
  - family: Chen
    given: Yii-Der Ida
  - family: Rich
    given: Stephen S.
  - family: McKean-Cowdin
    given: Roberta
  - family: Grallert
    given: Harald
  - family: Cheng
    given: Ching-Yu
  - family: Ghanbari
    given: Mohsen
  - family: Tai
    given: E-Shyong
  - family: Dupuis
    given: Josee
  - family: Kato
    given: Norihiro
  - family: Laakso
    given: Markku
  - family: Köttgen
    given: Anna
  - family: Koh
    given: Woon-Puay
  - family: Bowden
    given: Donald W.
  - family: Palmer
    given: Colin N. A.
  - family: Kooner
    given: Jaspal S.
  - family: Kooperberg
    given: Charles
  - family: Liu
    given: Simin
  - family: North
    given: Kari E.
  - family: Saleheen
    given: Danish
  - family: Hansen
    given: Torben
  - family: Pedersen
    given: Oluf
  - family: Wareham
    given: Nicholas J.
  - family: Lee
    given: Juyoung
  - family: Kim
    given: Bong-Jo
  - family: Millwood
    given: Iona Y.
  - family: Walters
    given: Robin G.
  - family: Stefansson
    given: Kari
  - family: Ahlqvist
    given: Emma
  - family: Goodarzi
    given: Mark O.
  - family: Mohlke
    given: Karen L.
  - family: Langenberg
    given: Claudia
  - family: Haiman
    given: Christopher A.
  - family: Loos
    given: Ruth J. F.
  - family: Florez
    given: Jose C.
  - family: Rader
    given: Daniel J.
  - family: Ritchie
    given: Marylyn D.
  - family: Zöllner
    given: Sebastian
  - family: Mägi
    given: Reedik
  - family: Marston
    given: Nicholas A.
  - family: Ruff
    given: Christian T.
  - family: Van Heel
    given: David A.
  - family: Finer
    given: Sarah
  - family: Denny
    given: Joshua C.
  - family: Yamauchi
    given: Toshimasa
  - family: Kadowaki
    given: Takashi
  - family: Chambers
    given: John C.
  - family: Ng
    given: Maggie C. Y.
  - family: Sim
    given: Xueling
  - family: Below
    given: Jennifer E.
  - family: Tsao
    given: Philip S.
  - family: Chang
    given: Kyong-Mi
  - family: McCarthy
    given: Mark I.
  - family: Meigs
    given: James B.
  - family: Mahajan
    given: Anubha
  - family: Spracklen
    given: Cassandra N.
  - family: Mercader
    given: Josep M.
  - family: Boehnke
    given: Michael
  - family: Rotter
    given: Jerome I.
  - family: Vujkovic
    given: Marijana
  - family: Voight
    given: Benjamin F.
  - family: Morris
    given: Andrew P.
  - family: Zeggini
    given: Eleftheria
  container-title: Nature
  doi: 10.1038/s41586-024-07019-6
  id: suzuki_genetic_2024
  issn: 0028-0836, 1476-4687
  issue: 8003
  issued: 2024-03
  page: 347-357
  title: Genetic drivers of heterogeneity in type 2 diabetes
    pathophysiology
  type: article-journal
  url: "https://www.nature.com/articles/s41586-024-07019-6"
  volume: 627
  journal-title: '*Nature*'
  date: 2024-03
  path: https://doi.org/10.1038/s41586-024-07019-6
  position: '91/365'
  first: '&emsp;&emsp;&emsp;'
- abstract: We postulated that T2D predisposes to exocrine pancreatic
    diseases through (epi)genetic mechanisms. We explored the methylome
    (methylationEPIC arrays) of the exocrine pancreas of 141 donors,
    assessing the impact of T2D. Epigenome-wide association study (EWAS)
    for T2D identified a hypermethylation in an enhancer of the
    Pancreatic-Lipase-Related-Protein 1 (PNLIPRP1) gene, associated with
    decreased PNLIPRP1 expression. PNLIPRP1 null variants (in 191K
    participants of the UKbiobank) associated with elevated glycemia and
    LDL-cholesterol. Mendelian Randomisation using 2.5M SNP OmniArrays
    in 111 donors evidenced that T2D was causal of PNLIPRP1
    hypermethylation, which was causal for LDL-cholesterol. Further
    AR42J rat exocrine cell studies demonstrated that Pnliprp1 knockdown
    induced acinar-to-ductal metaplasia, a known pre-pancreatic cancer
    state, and increased cholesterol levels, reversible with statin.
    This (epi)genetic study suggests a role for PNLIPRP1 in human
    metabolism and on exocrine pancreas function with potential
    implications for pancreatic diseases.
  accessed: 2024-09-13
  author:
  - family: Maurin
    given: Lucas
  - family: Marselli
    given: Lorella
  - family: Boissel
    given: Mathilde
  - family: Ning
    given: Lijiao
  - family: Boutry
    given: Raphael
  - family: Fernandes
    given: Justine
  - family: Suleiman
    given: Mara
  - family: De Luca
    given: Carmela
  - family: Leloire
    given: Audrey
  - family: Pascat
    given: Vincent
  - family: Toussaint
    given: Bénédicte
  - family: Amanzougarene
    given: Souhila
  - family: Derhourhi
    given: Mehdi
  - family: Jörns
    given: Anne
  - family: Lenzen
    given: Sigurd
  - family: Pattou
    given: François
  - family: Kerr-Conte
    given: Julie
  - family: Canouil
    given: Mickaël
  - family: Marchetti
    given: Piero
  - family: Bonnefond
    given: Amélie
  - family: Froguel
    given: Philippe
  - family: Khamis
    given: Amna
  container-title: Diabetes
  doi: 10.2337/db24-0215
  id: maurin_pnliprp1_2024
  issn: 0012-1797, 1939-327X
  issued: 2024-08
  page: db240215
  title: "*PNLIPRP1* hypermethylation in exocrine pancreas links type 2
    diabetes and cholesterol metabolism"
  type: article-journal
  url: "https://diabetesjournals.org/diabetes/article/doi/10.2337/db24-0215/157087/PNLIPRP1-hypermethylation-in-exocrine-pancreas"
  journal-title: '*Diabetes*'
  date: 2024-08
  path: https://doi.org/10.2337/db24-0215
  position: '18/22'
  first: '&emsp;&emsp;&emsp;'
- abstract: AbstractGenetic effects on changes in human traits over time
    are understudied and may have important pathophysiological impact.
    We propose a framework that enables data quality control, implements
    mixed models to evaluate trajectories of change in traits, and
    estimates phenotypes to identify age-varying genetic effects in
    GWAS. Using childhood BMI as an example trait, we included 71,336
    participants from six cohorts and estimated the slope and area under
    the BMI curve within four time periods (infancy, early childhood,
    late childhood and adolescence) for each participant, in addition to
    the age and BMI at the adiposity peak and the adiposity rebound.
    GWAS of the 12 estimated phenotypes identified 28 genome-wide
    significant variants at 13 loci, one of which (in DAOA) has not been
    previously associated with childhood or adult BMI. Genetic studies
    of changes in human traits over time could uncover unique biological
    mechanisms influencing quantitative traits.
  accessed: 2024-11-28
  author:
  - family: Burrows
    given: Kimberley
  - family: Heiskala
    given: Anni
  - family: Bradfield
    given: Jonathan P.
  - family: Balkhiyarova
    given: Zhanna
  - family: Ning
    given: Lijiao
  - family: Boissel
    given: Mathilde
  - family: Chan
    given: Yee-Ming
  - family: Froguel
    given: Philippe
  - family: Bonnefond
    given: Amelie
  - family: Hakonarson
    given: Hakon
  - family: Alves
    given: Alexessander Couto
  - family: Lawlor
    given: Deborah A.
  - family: Kaakinen
    given: Marika
  - family: Järvelin
    given: Marjo-Riitta
  - family: Grant
    given: Struan F. A.
  - family: Tilling
    given: Kate
  - family: Prokopenko
    given: Inga
  - family: Sebert
    given: Sylvain
  - family: Canouil
    given: Mickaël
  - family: Warrington
    given: Nicole M.
  container-title: Nature Communications
  doi: 10.1038/s41467-024-53687-3
  id: burrows_framework_2024
  issn: 2041-1723
  issue: 1
  issued: 2024-11
  page: 10067
  title: A framework for conducting GWAS using repeated measures data
    with an application to childhood BMI
  type: article-journal
  url: "https://www.nature.com/articles/s41467-024-53687-3"
  volume: 15
  journal-title: '*Nature Communications*'
  date: 2024-11
  path: https://doi.org/10.1038/s41467-024-53687-3
  position: '19/20'
  first: '&emsp;&emsp;&emsp;'