ACC2 gene polymorphisms,metabolic syndrome,and gene-nutrient interactions with dietary fat |
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| Authors: | Catherine M. Phillips Louisa Goumidi Sandrine Bertrais Martyn R. Field L. Adrienne Cupples Jose M. Ordovas Jolene McMonagle Catherine Defoort Julie A. Lovegrove Christian A. Drevon Ellen E. Blaak Beata Kiec-Wilk Ulf Riserus Jose Lopez-Miranda Ross McManus Serge Hercberg Denis Lairon Richard Planells Helen M. Roche |
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| Affiliation: | 1. Nutrigenomics Research Group, UCD School of Public Health and Population Science, UCD Conway Institute, University College Dublin, Dublin, Ireland;2. INSERM 476/INRA 1260, Université de la Méditerranée, Faculté de Médecine, Marseille, France;4. INSERM U557/INRA/CNAM, Université Paris, Bobigny, France;7. Hitachi Dublin Laboratory, Dublin, Ireland;11. Boston University School of Public Health, Boston, MA;8. Nutrition and Genomics Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA;71. Hugh Sinclair Unit of Human Nutrition, Department of Food Biosciences, Institute for Cardiovascular and Metabolic Research, University of Reading, Reading, UK;112. Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway;84. Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht, The Netherlands;77. Department of Clinical Biochemistry, Jagiellonian University Medical College, Krakow, Poland;1111. Department of Public Health and Caring Sciences/Clinical Nutrition and Metabolism, Uppsala University, Uppsala, Sweden;88. Lipids and Atherosclerosis Unit, Instituto Maimonides de Investigación Biomédica de Córdoba (IMIBIC)/Hospital Universitario Reina Sofía/Universidad de Córdoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Spain;771. Institute of Molecular Medicine, Trinity College Dublin, Dublin, Ireland |
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| Abstract: | Acetyl-CoA carboxylase β (ACC2) plays a key role in fatty acid synthesis and oxidation pathways. Disturbance of these pathways is associated with impaired insulin responsiveness and metabolic syndrome (MetS). Gene-nutrient interactions may affect MetS risk. This study determined the relationship between ACC2 polymorphisms (rs2075263, rs2268387, rs2284685, rs2284689, rs2300453, rs3742023, rs3742026, rs4766587, and rs6606697) and MetS risk, and whether dietary fatty acids modulate this in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1754). Minor A allele carriers of rs4766587 had increased MetS risk (OR 1.29 [CI 1.08, 1.58], P = 0.0064) compared with the GG homozygotes, which may in part be explained by their increased body mass index (BMI), abdominal obesity, and impaired insulin sensitivity (P < 0.05). MetS risk was modulated by dietary fat intake (P = 0.04 for gene-nutrient interaction), where risk conferred by the A allele was exacerbated among individuals with a high-fat intake (>35% energy) (OR 1.62 [CI 1.05, 2.50], P = 0.027), particularly a high intake (>5.5% energy) of n-6 polyunsaturated fat (PUFA) (OR 1.82 [CI 1.14, 2.94], P = 0.01; P = 0.05 for gene-nutrient interaction). Saturated and monounsaturated fat intake did not modulate MetS risk. Importantly, we replicated some of these findings in an independent cohort. In conclusion, the ACC2 rs4766587 polymorphism influences MetS risk, which was modulated by dietary fat, suggesting novel gene-nutrient interactions. |
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| Keywords: | genetic polymorphisms insulin resistance fatty acid metabolism polyunsaturated fatty acids |
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