Contributors: Institute of Metabolic Science; MRC; Departments of Epidemiology and Nutrition; Harvard School of Public Health; Department of Clinical Sciences; Skane University Hospital Lund; Division of Epidemiology and Community Health; University of Minnesota Twin Cities (UMN); University of Minnesota System (UMN)-University of Minnesota System (UMN); Division of Cardiology; Duke University Medical Center; Brigham and Women's Hospital Boston; Institute of Health Sciences and Biocenter Oulu; University of Oulu; Hagedorn Research Institute; Else Kroener Fresenius Centre - Zentralinstitut für Ernährungs und Lebensmittelfors (ZIEL); Technische Universität Munchen - Technical University Munich - Université Technique de Munich (TUM); Department of Population Health Sciences; University of Wisconsin-Madison; Institute of Epidemiology Neuherberg (EPI); German Research Center for Environmental Health - Helmholtz Center München (GmbH); Centre for Paediatric Epidemiology and Biostatistics; University College of London London (UCL); MRC Centre for Epidemiology of Child Health; UCL Institute of Child Health; Institut de biologie de Lille - UMS 3702 (IBL); Institut Pasteur de Lille; Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Université de Lille-Centre National de la Recherche Scientifique (CNRS); Department of Medical Genetics; Université de Lausanne = University of Lausanne (UNIL); Department of Epidemiology and Public Health; Department of Medicine; University of Eastern Finland-Kuopio University Hospital (KUH); Department of Epidemiology; Deutsches Institut für Ernährungsforschung Potsdam-Rehbrücke (DifE); Leibniz Association-Leibniz Association; Centre de recherche en épidémiologie et santé des populations (CESP); Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM); National University of Singapore (NUS)-Yong Loo Lin School of Medicine; King‘s College London; Centre for Causal Analyses in Translational Epidemiology; University of Bristol Bristol -Medical Research Council; Division of Preventive Medicine; Netherlands Genomics Initiative; Netherlands Consortium for Healthy Aging Leiden, Netherlands (NCHA); Department of Internal Medicine; Erasmus University Medical Center Rotterdam (Erasmus MC); The Biostatistics Center; The George Washington University (GW); National Institute on Aging Bethesda, USA (NIA); National Institutes of Health Bethesda, MD, USA (NIH); Mental Health Sciences Unit; Department of Clinical Medicine; University of Bergen (UiB); Department of Biostatistics and Center for Statistical Genetics; University of Michigan Ann Arbor; University of Michigan System-University of Michigan System; Department of Genetics; University of North Carolina Chapel Hill (UNC); University of North Carolina System (UNC)-University of North Carolina System (UNC); Molecular Genetics Section; University of Groningen Groningen -University Medical Centre Groningen; Complex Genetics Section; University Medical Center Utrecht; Julius Center for Health Sciences and Primary Care; Institute of Preventive Medicine; Copenhagen University Hospital; Department of Biomedical Sciences Copenhagen; Faculty of Health and Medical Sciences; University of Copenhagen = Københavns Universitet (UCPH)-University of Copenhagen = Københavns Universitet (UCPH); Genetic Epidemiology Unit; Medstar Research Institute; Division of Endocrinology, Diabetology, Nephrology, Vascular Disease, and Clinical Chemistry; Eberhard Karls Universität Tübingen = Eberhard Karls University of Tuebingen; Department of Nutrition-Dietetics; Harokopio University of Athens; Division of Statistical Genomics; Washington University School of Medicine in St. Louis; Washington University in Saint Louis (WUSTL)-Washington University in Saint Louis (WUSTL); University of Maryland School of Medicine; University of Maryland System; Unit for Preventive Nutrition; Karolinska Institutet Stockholm; Department of Physical Education and Sport; Universidad de Granada = University of Granada (UGR); Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas; Hospital Clínico San Carlos; Department of Physiology; University of Eastern Finland-Institute of Biomedicine; The Research Centre of Applied and Preventive Cardiovascular Medicine; University of Turku
نبذة مختصرة : International audience ; BACKGROUND: The FTO gene harbors the strongest known susceptibility locus for obesity. While many individual studies have suggested that physical activity (PA) may attenuate the effect of FTO on obesity risk, other studies have not been able to confirm this interaction. To confirm or refute unambiguously whether PA attenuates the association of FTO with obesity risk, we meta-analyzed data from 45 studies of adults (n = 218,166) and nine studies of children and adolescents (n = 19,268). METHODS AND FINDINGS: All studies identified to have data on the FTO rs9939609 variant (or any proxy [r(2)>0.8]) and PA were invited to participate, regardless of ethnicity or age of the participants. PA was standardized by categorizing it into a dichotomous variable (physically inactive versus active) in each study. Overall, 25% of adults and 13% of children were categorized as inactive. Interaction analyses were performed within each study by including the FTO×PA interaction term in an additive model, adjusting for age and sex. Subsequently, random effects meta-analysis was used to pool the interaction terms. In adults, the minor (A-) allele of rs9939609 increased the odds of obesity by 1.23-fold/allele (95% CI 1.20-1.26), but PA attenuated this effect (p(interaction) = 0.001). More specifically, the minor allele of rs9939609 increased the odds of obesity less in the physically active group (odds ratio = 1.22/allele, 95% CI 1.19-1.25) than in the inactive group (odds ratio = 1.30/allele, 95% CI 1.24-1.36). No such interaction was found in children and adolescents. CONCLUSIONS: The association of the FTO risk allele with the odds of obesity is attenuated by 27% in physically active adults, highlighting the importance of PA in particular in those genetically predisposed to obesity.
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