PuSH - Publikationsserver des Helmholtz Zentrums München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Horikoshi, M.* ; Beaumont, R.N.* ; Day, F.R.* ; Warrington, N.M.* ; Kooijman, M.N.* ; Fernandez-Tajes, J.* ; Feenstra, B.* ; van Zuydam, N.R.* ; Gaulton, K.J.* ; Grarup, N.* ; Bradfield, J.P.* ; Strachan, D.P.* ; Li-Gao, R.* ; Ahluwalia, T.S.* ; Kreiner, E.* ; Rueedi, R.* ; Lyytikäinen, L.-P.* ; Cousminer, D.L.* ; Wu, Y.* ; Thiering, E. ; Wang, C.A.* ; Have, C.T.* ; Hottenga, J.J.* ; Vilor-Tejedor, N.* ; Joshi, P.K.* ; Boh, E.T.* ; Ntalla, I.* ; Pitkänen, N.* ; Mahajan, A.* ; van Leeuwen, E.M.* ; Joro, R.* ; Lagou, V.* ; Nodzenski, M.* ; Diver, L.A.* ; Zondervan, K.T.* ; Bustamante, M.* ; Marques-Vidal, P.* ; Mercader, J.M.* ; Bennett, A.J.* ; Rahmioglu, N.* ; Nyholt, D.R.* ; Ma, R.C.* ; Tam, C.H.* ; Tam, W.H.* ; Ganesh, S.K.* ; van Rooij, F.J.* ; Jones, S.E.* ; Loh, P.R.* ; Ruth, K.S.* ; Tuke, M.A.* ; Tyrrell, J.* ; Wood, A.R.* ; Yaghootkar, H.* ; Scholtens, D.M.* ; Paternoster, L.* ; Prokopenko, I.* ; Kovacs, P.* ; Atalay, M.* ; Willems, S.M.* ; Panoutsopoulou, K.* ; Wang, X.* ; Carstensen, L.* ; Geller, F.* ; Schraut, K.E.* ; Murcia, M.* ; van Beijsterveldt, C.E.* ; Willemsen, G.* ; Appel, E.V.* ; Fonvig, C.E.* ; Trier, C.* ; Tiesler, C.M. ; Standl, M. ; Kutalik, Z.* ; Bonàs-Guarch, S.* ; Hougaard, D.M.* ; Sánchez, F.* ; Torrents, D.* ; Waage, J.* ; Hollegaard, M.V.* ; de Haan, H.G.* ; Rosendaal, F.R.* ; Medina-Gomez, C.* ; Ring, S.M.* ; Hemani, G.* ; McMahon, G.* ; Robertson, N.R.* ; Groves, C.J.* ; Langenberg, C.* ; Luan, J.* ; Scott, R.A.* ; Zhao, J.H.* ; Mentch, F.D.* ; MacKenzie, S.M.* ; Reynolds, R.M.* ; Lowe, W.L.* ; Tönjes, A.* ; Stumvoll, M.* ; Lindi, V.* ; Lakka, T.A.* ; van Duijn, C.M.* ; Kiess, W.* ; Körner, A.* ; Sørensen, T.I.* ; Niinikoski, H.* ; Pahkala, K.* ; Raitakari, O.T.* ; Zeggini, E.* ; Dedoussis, G.V.* ; Teo, Y.Y.* ; Saw, S.M.* ; Melbye, M.* ; Campbell, H.* ; Wilson, J.F.* ; Vrijheid, M.* ; de Geus, E.J.* ; Boomsma, D.I.* ; Kadarmideen, H.N.* ; Holm, J.C.* ; Hansen, T.* ; Sebert, S.* ; Hattersley, A.T.* ; Beilin, L.J.* ; Newnham, J.P.* ; Pennell, C.E.* ; Heinrich, J. ; Adair, L.S.* ; Borja, J.B.* ; Mohlke, K.L.* ; Eriksson, J.G.* ; Widen, E.* ; Kähönen, M.* ; Viikari, J.S.* ; Lehtimäki, T.* ; Vollenweider, P.* ; Bønnelykke, K.* ; Bisgaard, H.* ; Mook-Kanamori, D.O.* ; Hofman, A.* ; Rivadeneira, F.* ; Uitterlinden, A.G.* ; Pisinger, C.* ; Pedersen, O.* ; Power, C.* ; Hyppönen, E.* ; Wareham, N.J.* ; Hakonarson, H.* ; Davies, E.* ; Walker, B.R.* ; Jaddoe, V.W.* ; Jarvelin, M.R.* ; Grant, S.F.* ; Vaag, A.A.* ; Lawlor, D.A.* ; Frayling, T.M.* ; Smith, G.D.* ; Morris, A.P.* ; Ong, K.K.* ; Felix, J.F.* ; Timpson, N.J.* ; Perry, J.R.* ; Evans, D.M* ; McCarthy, M.I.* ; Freathy, R.M.*

Genome-wide associations for birth weight and correlations with adult disease.

Nature 538, 248-252 (2016)
Postprint Forschungsdaten DOI PMC
Open Access Green
Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW (P < 5 × 10(-8)). Overall, approximately 15% of variance in BW was captured by assays of fetal genetic variation. Using genetic association alone, we found strong inverse genetic correlations between BW and systolic blood pressure (Rg = -0.22, P = 5.5 × 10(-13)), T2D (Rg = -0.27, P = 1.1 × 10(-6)) and coronary artery disease (Rg = -0.30, P = 6.5 × 10(-9)). In addition, using large -cohort datasets, we demonstrated that genetic factors were the major contributor to the negative covariance between BW and future cardiometabolic risk. Pathway analyses indicated that the protein products of genes within BW-associated regions were enriched for diverse processes including insulin signalling, glucose homeostasis, glycogen biosynthesis and chromatin remodelling. There was also enrichment of associations with BW in known imprinted regions (P = 1.9 × 10(-4)). We demonstrate that life-course associations between early growth phenotypes and adult cardiometabolic disease are in part the result of shared genetic effects and identify some of the pathways through which these causal genetic effects are mediated.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Scopus
Cited By
Altmetric
38.138
8.377
231
241
Tags
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern

Zusatzinfos bearbeiten
Eigene Tags bearbeiten
Privat
Eigene Anmerkung bearbeiten
Privat
Auf Publikationslisten für
Homepage nicht anzeigen
Als besondere Publikation
markieren
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Blood-pressure; Altitude Adaptation; Genotype Imputation; Gene-expression; Human Height; Metaanalysis; Traits; Loci; Population; Variants
Sprache englisch
Veröffentlichungsjahr 2016
HGF-Berichtsjahr 2016
ISSN (print) / ISBN 0028-0836
e-ISSN 1476-4687
Zeitschrift Nature
Quellenangaben Band: 538, Heft: 7624, Seiten: 248-252 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology (EPI)
POF Topic(s) 30503 - Chronic Diseases of the Lung and Allergies
Forschungsfeld(er) Genetics and Epidemiology
PSP-Element(e) G-503900-001
DOI 10.1038/nature19806
WOS ID WOS:000386671000046
Scopus ID 84991665514
PubMed ID 27680694
Erfassungsdatum 2016-10-13
[➜Korrektur melden]