期刊
JOURNAL OF LIPID RESEARCH
卷 51, 期 7, 页码 1793-1800出版社
ELSEVIER
DOI: 10.1194/jlr.M003046
关键词
genetic polymorphisms; insulin resistance; fatty acid metabolism; PUFA
资金
- European Commission [FOOD-CT-2003-505944]
- Norwegian Foundation for Health and Rehabilitation
- South-Eastern Norway Regional Health Authority
- Johan Throne Holst Foundation for Nutrition Research
- Freia Medical Research Foundation
Long-chain acyl CoA synthetase 1 (ACSL1) plays an important role in fatty acid metabolism and triacylglycerol (TAG) synthesis. Disturbance of these pathways may result in dyslipidemia and insulin resistance, hallmarks of the metabolic syndrome (MetS). Dietary fat is a key environmental factor that may interact with genetic determinants of lipid metabolism to affect MetS risk. We investigated the relationship between ACSL1 polymorphisms (rs4862417, rs6552828, rs13120078, rs9997745, and rs12503643) and MetS risk and determined potential interactions with dietary fat in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1,754). GG homozygotes for rs9997745 had increased MetS risk {odds ratio (OR) 1.90 [ confidence interval (CI) 1.15, 3.13]; P = 0.01}, displayed elevated fasting glucose (P = 0.001) and insulin concentrations (P = 0.002) and increased insulin resistance (P = 0.03) relative to the A allele carriers. MetS risk was modulated by dietary fat, whereby the risk conferred by GG homozygosity was abolished among individuals consuming either a low-fat (< 35% energy) or a high-PUFA diet (>5.5% energy). In conclusion, ACSL1 rs9997745 influences MetS risk, most likely via disturbances in fatty acid metabolism, which was modulated by dietary fat consumption, particularly PUFA intake, suggesting novel gene-nutrient interactions.-Phillips, C. M., L. Goumidi, S. Bertrais, M. R. Field, L. A. Cupples, J. M. Ordovas, C. Defoort, J. A. Lovegrove, C. A. Drevon, M. J. Gibney, E. E. Blaak, B. Kiec-Wilk, B. Karlstrom, J. Lopez-Miranda, R. McManus, S. Hercberg, D. Lairon, R. Planells, and H. M. Roche. Gene-nutrient interactions with dietary fat modulate the association between genetic variation of the ACSL1 gene and metabolic syndrome. J. Lipid Res. 2010. 51: 1793-1800.
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