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Biochemical, Molecular, and Genetic Mechanisms

Dietary Saturated Fat Modulates the Association between STAT3 Polymorphisms and Abdominal Obesity in Adults^1,2

³ Nutrigenomics Research Group, School of Public Health and Population Science, University College Dublin Conway Institute, University College, Dublin 4, Ireland; ⁴ Institut national de la santé et de la recherche médicale, 476 Lipid nutrients and prevention of metabolic diseases; Institut National de la Recherche Agronomique, 1260; Université de la Méditerranée, Faculté de Médecine, 13385 Marseille Cedex 05, France; ⁵ Institut national de la santé et de la recherche médicale, U557; Institut National de la Recherche Agronomique; Conservatoire National des Arts et Métiers; Université Paris 13, F-93017 Bobigny, France; ⁶ Hitachi Dublin Laboratory, Dublin 2, Ireland; ⁷ Boston University School of Public Health, Boston, MA 02118; ⁸ Nutrition and Genomics Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111; and ⁹ Institute of Molecular Medicine, Trinity College, Dublin 8, Ireland

Signal transducer and activator of transcription 3 (STAT3) plays a key role in body weight regulation and glucose homeostasis, 2 important determinants of metabolic syndrome (MetS). Dietary fat is a key environmental factor that may interact with genotype to affect MetS risk. In this study, we investigated the relationship between STAT3 polymorphisms and MetS phenotypes and determined potential interactions with dietary fatty acids. STAT3 polymorphisms (rs8069645, rs744166, rs2306580, rs2293152, and rs10530050), biochemical measurements, and dietary fat composition were determined in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1754). STAT3 polymorphisms were not associated with MetS risk. However, minor G allele carriers for rs8069645, rs744166, and rs1053005 and major GG homozygotes for rs2293152 had increased risk of abdominal obesity compared with noncarriers [odds ratio (OR) = 2.22, P = 0.0005; OR = 2.08, P = 0.0017; OR = 2.00, P = 0.0033; and OR = 1.95, P = 0.028, respectively]. The number of risk alleles additively increased obesity risk (P = 0.0003). Dietary SFA intake exacerbated these effects; among all participants with the highest SFA intake (15.5% of energy), individuals carrying >2 risk alleles had further increased risk of obesity (OR = 3.30; 95% CI = 1.50–7.28; P = 0.0079) compared with those carrying 1 risk allele. Interaction analysis confirmed this gene-nutrient interaction whereby increasing SFA intake was predictive of increased waist circumference (P = 0.038). In conclusion, STAT3 gene polymorphisms influenced the risk of abdominal obesity, which is modulated by dietary SFA intake, suggesting novel gene-nutrient interactions.

^* To whom correspondence should be addressed. E-mail: helen.roche{at}ucd.ie.

Manuscript received 25 May 2009. Initial review completed 8 July 2009. Revision accepted 24 August 2009.

Published online 23 September 2009.