Sofus C Larsen1, Lars Ängquist2, Jane N Østergaard3, Tarunveer S Ahluwalia4, Karani S Vimaleswaran5, Nina Roswall6, Lotte M Mortensen7, Birgit M Nielsen8, Anne Tjønneland6, Nicholas J Wareham9, Domenico Palli10, Giovanna Masala10, Wim H M Saris11, Daphne L van der A12, Jolanda M A Boer12, Edith J M Feskens13, Heiner Boeing14, Marianne U Jakobsen15, Ruth J F Loos16, Thorkild I A Sørensen17, Kim Overvad7. 1. Research Unit for Dietary Studies at the Parker Institute, Institute of Preventive Medicine, Bispebjerg and Frederiksberg Hospitals, The Capital Region, Copenhagen, Denmark; Department of Cardiology, Cardiovascular Research Center, Aalborg University Hospital, Aalborg, Denmark; sofus.christian.larsen@regionh.dk. 2. Institute of Preventive Medicine, Bispebjerg and Frederiksberg Hospitals, The Capital Region, Copenhagen, Denmark; 3. Department of Cardiology, Cardiovascular Research Center, Aalborg University Hospital, Aalborg, Denmark; Department for Health and Care, Aarhus Municipality, Aarhus, Denmark; Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark; 4. Novo Nordisk Foundation Center for Basic Metabolic Research, and Department of Public Health, Faculty of Health and Medical Sciences, Copenhagen Prospective Studies on Asthma in Childhood (COPSAC), Herlev and Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark; Steno Diabetes Center, Gentofte, Denmark; 5. Hugh Sinclair Unit of Human Nutrition, Department of Food and Nutritional Sciences, Institute for Cardiovascular and Metabolic Research (ICMR), University of Reading, Reading, United Kingdom; Medical Research Council (MRC) Epidemiology Unit, Cambridge, United Kingdom; 6. Danish Cancer Society Research Center, Danish Cancer Society, Copenhagen, Denmark; 7. Department of Cardiology, Cardiovascular Research Center, Aalborg University Hospital, Aalborg, Denmark; Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark; 8. Institute of Preventive Medicine, Bispebjerg and Frederiksberg Hospitals, The Capital Region, Copenhagen, Denmark; Copenhagen Prospective Studies on Asthma in Childhood (COPSAC), Herlev and Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark; 9. MRC Epidemiology Unit, Institute of Metabolic Science, Addenbrookes Hospital, Cambridge, United Kingdom; 10. Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute (ISPO), Florence, Italy; 11. Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Centre, Maastricht, Netherlands; 12. National Institute for Public Health and the Environment (RIVM), Bilthoven, Netherlands; 13. Division of Human Nutrition, Wageningen University, Wageningen, Netherlands; 14. Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany; 15. Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark; 16. MRC Epidemiology Unit, Institute of Metabolic Science, University of Cambridge, Cambridge, United Kingdom; Charles Bronfman Institute for Personalized Medicine, Department of Preventive Medicine, and the Mindich Child Health and Development Institute, The Icahn School of Medicine at Mount Sinai, New York, NY; and. 17. Institute of Preventive Medicine, Bispebjerg and Frederiksberg Hospitals, The Capital Region, Copenhagen, Denmark; Novo Nordisk Foundation Center for Basic Metabolic Research, and Department of Public Health, Faculty of Health and Medical Sciences, MRC Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom.
Abstract
BACKGROUND: Although the peroxisome proliferator-activated receptor γ (PPARγ) pathway is central in adipogenesis, it remains unknown whether it influences change in body weight (BW) and whether dietary fat has a modifying effect on the association. OBJECTIVES: We examined whether 27 single nucleotide polymorphisms (SNPs) within 4 genes in the PPARγ pathway are associated with the OR of being a BW gainer or with annual changes in anthropometry and whether intake of total fat, monounsaturated fat, polyunsaturated fat, or saturated fat has a modifying effect on these associations. METHODS: A case-noncase study included 11,048 men and women from cohorts in the European Diet, Obesity and Genes study; 5552 were cases, defined as individuals with the greatest BW gain during follow-up, and 6548 were randomly selected, including 5496 noncases. We selected 4 genes [CCAAT/enhancer binding protein β (CEBPB), phosphoenolpyruvate carboxykinase 2, PPARγ gene (PPARG), and sterol regulatory element binding transcription factor 1] according to evidence about biologic plausibility for interactions with dietary fat in weight regulation. Diet was assessed at baseline, and anthropometry was followed for 7 y. RESULTS: The ORs for being a BW gainer for the 27 genetic variants ranged from 0.87 (95% CI: 0.79, 1.03) to 1.12 (95% CI: 0.96, 1.22) per additional minor allele. Uncorrected, CEBPB rs4253449 had a significant interaction with the intake of total fat and subgroups of fat. The OR for being a BW gainer for each additional rs4253449 minor allele per 100 kcal higher total fat intake was 1.07 (95% CI: 1.02, 1.12; P = 0.008), and similar associations were found for subgroups of fat. CONCLUSIONS: Among European men and women, the influence of dietary fat on associations between SNPs in the PPARγ pathway and anthropometry is likely to be absent or marginal. The observed interaction between rs4253449 and dietary fat needs confirmation.
BACKGROUND: Although the peroxisome proliferator-activated receptor γ (PPARγ) pathway is central in adipogenesis, it remains unknown whether it influences change in body weight (BW) and whether dietary fat has a modifying effect on the association. OBJECTIVES: We examined whether 27 single nucleotide polymorphisms (SNPs) within 4 genes in the PPARγ pathway are associated with the OR of being a BW gainer or with annual changes in anthropometry and whether intake of total fat, monounsaturated fat, polyunsaturated fat, or saturated fat has a modifying effect on these associations. METHODS: A case-noncase study included 11,048 men and women from cohorts in the European Diet, Obesity and Genes study; 5552 were cases, defined as individuals with the greatest BW gain during follow-up, and 6548 were randomly selected, including 5496 noncases. We selected 4 genes [CCAAT/enhancer binding protein β (CEBPB), phosphoenolpyruvate carboxykinase 2, PPARγ gene (PPARG), and sterol regulatory element binding transcription factor 1] according to evidence about biologic plausibility for interactions with dietary fat in weight regulation. Diet was assessed at baseline, and anthropometry was followed for 7 y. RESULTS: The ORs for being a BW gainer for the 27 genetic variants ranged from 0.87 (95% CI: 0.79, 1.03) to 1.12 (95% CI: 0.96, 1.22) per additional minor allele. Uncorrected, CEBPB rs4253449 had a significant interaction with the intake of total fat and subgroups of fat. The OR for being a BW gainer for each additional rs4253449 minor allele per 100 kcal higher total fat intake was 1.07 (95% CI: 1.02, 1.12; P = 0.008), and similar associations were found for subgroups of fat. CONCLUSIONS: Among European men and women, the influence of dietary fat on associations between SNPs in the PPARγ pathway and anthropometry is likely to be absent or marginal. The observed interaction between rs4253449 and dietary fat needs confirmation.
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