Genome-wide associations for birth weight and correlations with adult disease View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-10

AUTHORS

Momoko Horikoshi, Robin N. Beaumont, Felix R. Day, Nicole M. Warrington, Marjolein N. Kooijman, Juan Fernandez-Tajes, Bjarke Feenstra, Natalie R. van Zuydam, Kyle J. Gaulton, Niels Grarup, Jonathan P. Bradfield, David P. Strachan, Ruifang Li-Gao, Tarunveer S. Ahluwalia, Eskil Kreiner, Rico Rueedi, Leo-Pekka Lyytikäinen, Diana L. Cousminer, Ying Wu, Elisabeth Thiering, Carol A. Wang, Christian T. Have, Jouke-Jan Hottenga, Natalia Vilor-Tejedor, Peter K. Joshi, Eileen Tai Hui Boh, Ioanna Ntalla, Niina Pitkänen, Anubha Mahajan, Elisabeth M. van Leeuwen, Raimo Joro, Vasiliki Lagou, Michael Nodzenski, Louise A. Diver, Krina T. Zondervan, Mariona Bustamante, Pedro Marques-Vidal, Josep M. Mercader, Amanda J. Bennett, Nilufer Rahmioglu, Dale R. Nyholt, Ronald C. W., Claudia H. T. Tam, Hung Tam, CHARGE Consortium Hematology Working Group, Santhi K. Ganesh, Frank J. A. van Rooij, Samuel E. Jones, Po-Ru Loh, Katherine S. Ruth, Marcus A. Tuke, Jessica Tyrrell, Andrew R. Wood, Hanieh Yaghootkar, Denise M. Scholtens, Lavinia Paternoster, Inga Prokopenko, Peter Kovacs, Mustafa Atalay, Sara M. Willems, Kalliope Panoutsopoulou, Xu Wang, Lisbeth Carstensen, Frank Geller, Katharina E. Schraut, Mario Murcia, Catharina E. M. van Beijsterveldt, Gonneke Willemsen, Emil V. R. Appel, Cilius E. Fonvig, Caecilie Trier, Carla M. T. Tiesler, Marie Standl, Zoltán Kutalik, Sílvia Bonàs-Guarch, David M. Hougaard, Friman Sánchez, David Torrents, Johannes Waage, Mads V. Hollegaard, Hugoline G. de Haan, Frits R. Rosendaal, Carolina Medina-Gomez, Susan M. Ring, Gibran Hemani, George McMahon, Neil R. Robertson, Christopher J. Groves, Claudia Langenberg, Jian’an Luan, Robert A. Scott, Jing Hua Zhao, Frank D. Mentch, Scott M. MacKenzie, Rebecca M. Reynolds, Early Growth Genetics Consortium, William L. Lowe, Anke Tönjes, Michael Stumvoll, Virpi Lindi, Timo A. Lakka, Cornelia M. van Duijn, Wieland Kiess, Antje Körner, Thorkild I. A. Sørensen, Harri Niinikoski, Katja Pahkala, Olli T. Raitakari, Eleftheria Zeggini, George V. Dedoussis, Yik-Ying Teo, Seang-Mei Saw, Mads Melbye, Harry Campbell, James F. Wilson, Martine Vrijheid, Eco J. C. N. de Geus, Dorret I. Boomsma, Haja N. Kadarmideen, Jens-Christian Holm, Torben Hansen, Sylvain Sebert, Andrew T. Hattersley, Lawrence J. Beilin, John P. Newnham, Craig E. Pennell, Joachim Heinrich, Linda S. Adair, Judith B. Borja, Karen L. Mohlke, Johan G. Eriksson, Elisabeth Widén, Mika Kähönen, Jorma S. Viikari, Terho Lehtimäki, Peter Vollenweider, Klaus Bønnelykke, Hans Bisgaard, Dennis O. Mook-Kanamori, Albert Hofman, Fernando Rivadeneira, André G. Uitterlinden, Charlotta Pisinger, Oluf Pedersen, Christine Power, Elina Hyppönen, Nicholas J. Wareham, Hakon Hakonarson, Eleanor Davies, Brian R. Walker, Vincent W. V. Jaddoe, Marjo-Riitta Järvelin, Struan F. A. Grant, Allan A. Vaag, Debbie A. Lawlor, Timothy M. Frayling, George Davey Smith, Andrew P. Morris, Ken K. Ong, Janine F. Felix, Nicholas J. Timpson, John R. B. Perry, David M. Evans, Mark I. McCarthy, Rachel M. Freathy

ABSTRACT

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. More... »

PAGES

248

References to SciGraph publications

Journal

TITLE

Nature

ISSUE

7624

VOLUME

538

Author Affiliations

  • University of Oxford
  • University of Cambridge
  • University of Western Australia
  • Erasmus University Medical Center
  • Wellcome Centre for Human Genetics
  • Statens Serum Institut
  • University of California, San Diego
  • University of Copenhagen
  • Children's Hospital of Philadelphia
  • St George's, University of London
  • Leiden University Medical Center
  • Steno Diabetes Center
  • Swiss Institute of Bioinformatics
  • University of Tampere
  • University of Pennsylvania
  • University of North Carolina at Chapel Hill
  • Klinikum der Universität München
  • VU University Amsterdam
  • Instituto de Salud Carlos III
  • University of Edinburgh
  • National University of Singapore
  • Harokopio University
  • University of Turku
  • University of Eastern Finland
  • Flanders Institute for Biotechnology
  • Northwestern University
  • University of Glasgow
  • Centre for Genomic Regulation
  • University Hospital of Lausanne
  • Barcelona Supercomputing Center
  • Queensland University of Technology
  • Chinese University of Hong Kong
  • University of Michigan–Ann Arbor
  • Broad Institute
  • University of Exeter
  • University of Bristol
  • Imperial College London
  • Leipzig University
  • Wellcome Sanger Institute
  • Institute of Social and Preventive Medicine
  • Institució Catalana de Recerca i Estudis Avançats
  • Kuopion Liikuntalääketieteen Tutkimuslaitos
  • Turku University Hospital
  • Singapore Eye Research Institute
  • Stanford University
  • EMGO Institute for Health and Care Research
  • University of Oulu
  • University of North Carolina System
  • University of San Carlos
  • Folkhälsans Forskningscentrum
  • University of Helsinki
  • King Faisal Specialist Hospital & Research Centre
  • University College London
  • South Australian Health and Medical Research Institute
  • Oulu University Hospital
  • AstraZeneca (Sweden)
  • University of Tartu
  • Churchill Hospital
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature19806

    DOI

    http://dx.doi.org/10.1038/nature19806

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1047510296

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27680694


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        "description": "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\u2009<\u20095\u2009\u00d7\u200910-8). 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\u2009=\u2009-0.22, P\u2009=\u20095.5\u2009\u00d7\u200910-13), T2D (Rg\u2009=\u2009-0.27, P\u2009=\u20091.1\u2009\u00d7\u200910-6) and coronary artery disease (Rg\u2009=\u2009-0.30, P\u2009=\u20096.5\u2009\u00d7\u200910-9). 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\u2009=\u20091.9\u2009\u00d7\u200910-4). 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.", 
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