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ADIPOQ Polymorphisms, Monounsaturated Fatty Acids, and Obesity Risk: The GOLDN Study
Author(s) -
Warodomwichit Daruneewan,
Shen Jian,
Arnett Donna K.,
Tsai Michael Y.,
Kabagambe Edmond K.,
Peacock James M.,
Hixson James E.,
Straka Robert J.,
Province Michael A.,
An Ping,
Lai ChaoQiang,
Parnell Laurence D.,
Borecki Ingrid B.,
Ordovas Jose M.
Publication year - 2009
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2008.583
Subject(s) - adiponectin , medicine , endocrinology , single nucleotide polymorphism , obesity , odds ratio , waist , type 2 diabetes , metabolic syndrome , allele , genotype , confidence interval , diabetes mellitus , insulin resistance , biology , genetics , gene
Serum adiponectin levels have been positively associated with insulin sensitivity and are decreased in type 2 diabetes (T2D) and obesity. Genetic and environmental factors influence serum adiponectin and may contribute to risk of metabolic syndrome and T2D. Therefore, we investigated the effect of ADIPOQ single‐nucleotide polymorphisms (SNPs), −11377C>G and −11391G>A, on metabolic‐related traits, and their modulation by dietary fat in white Americans. Data were collected from 1,083 subjects participating in the Genetics of Lipid Lowering Drugs and Diet Network study. Mean serum adiponectin concentration was higher for carriers of the −11391A allele ( P = 0.001) but lower for the −11377G allele carriers ( P = 0.017). Moreover, we found a significant association with obesity traits for the −11391G>A SNP. Carriers of the −11391A allele had significantly lower weight ( P = 0.029), BMI ( P = 0.019), waist ( P = 0.003), and hip circumferences ( P = 0.004) compared to noncarriers. Interestingly, the associations of the −11391G>A with BMI and obesity risk were modified by monounsaturated fatty acids (MUFAs) intake ( P ‐interaction = 0.021 and 0.034 for BMI and obesity risk, respectively). In subjects with MUFA intake above the median (≥13% of energy intake), −11391A carriers had lower BMI (27.1 kg/m 2 for GA+AA vs. 29.1 kg/m 2 for GG, P = 0.002) and decreased obesity risk (odds ratio for −11391A = 0.52, 95% confidence interval (CI); 0.28–0.96; P = 0.031). However, we did not detect genotype‐related differences for BMI or obesity in subjects with MUFA intake <13%. Our findings support a significant association between the −11391G>A SNPs and obesity‐related traits and the potential to moderate such effects using dietary modification.