Document Detail


ACC2 gene polymorphisms, metabolic syndrome, and gene-nutrient interactions with dietary fat.
MedLine Citation:
PMID:  20855566     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
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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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-09-20
Journal Detail:
Title:  Journal of lipid research     Volume:  51     ISSN:  0022-2275     ISO Abbreviation:  J. Lipid Res.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-10     Completed Date:  2011-02-22     Revised Date:  2011-12-21    
Medline Journal Info:
Nlm Unique ID:  0376606     Medline TA:  J Lipid Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3500-7     Citation Subset:  IM    
Affiliation:
Nutrigenomics Research Group, UCD School of Public Health and Population Science, UCD Conway Institute, University College Dublin, Dublin, Ireland.
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MeSH Terms
Descriptor/Qualifier:
Acetyl-CoA Carboxylase / chemistry,  genetics*,  metabolism*
Alleles
Body Mass Index
Dietary Fats / administration & dosage,  metabolism*
Fatty Acids / metabolism
Fatty Acids, Unsaturated / metabolism
Genotype
Humans
Insulin Resistance
Metabolic Syndrome X / genetics*,  metabolism*
Obesity, Abdominal / genetics,  metabolism,  pathology
Polymorphism, Genetic*
Risk Factors
Chemical
Reg. No./Substance:
0/Dietary Fats; 0/Fatty Acids; 0/Fatty Acids, Unsaturated; EC 6.4.1.2/Acetyl-CoA Carboxylase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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