|Lai, Chao Qiang|
Submitted to: Obesity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/2/2008
Publication Date: 12/18/2008
Citation: Warodomwichit, D., Shen, J., Arnett, D., Tsai, M., Kabagambe, E., Peacock, J., Hixson, J., Straka, R., Province, M., An, P., Lai, C., Parnell, L.D., Borecki, I., Ordovas, J.M. 2009. ADIPOQ Polymorphisms, Monounsaturated Fatty Acids, and Obesity Risk: The GOLDN Study. Obesity. 17:510-517.
Interpretive Summary: Obesity is to related many diseases and health problems such as type 2 diabetes, dyslipidemia and cardiovascular disease and becomes a major health crisis in the United States. Genetic and environmental factors play a role in the development of obesity and other metabolic related phenotypes. The current study showed that the mutation at the ADIPOQ gene (-11391G>A) increased serum adiponectin, and decreased obesity traits. Moreover, researchers observed that dietary fatty acids modulate the genetic effect on obesity. The beneficial effects of the ADIPOQ variant were found among subjects with high monounsaturated fatty acids intake, showing the potential of healthy dietary habits. The findings support the importance of gene and diet interaction in relation to obesity.
Technical Abstract: Objective: To explore whether dietary fat modulates the association of genetic variations at ADIPOQ locus with obesity traits in White US subjects. Methods and Procedures: we genotyped two promoter single nucleotide polymorphisms (SNPs) at adiponectin gene, -11391G>A and -1137C>G, in 1083 participants (515 men and 568 women) in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) Study. Dietary intake, anthropometric and biochemical variables and serum adiponectin were assessed. Results: Serum adiponectin was higher for carriers of the -11391A allele (P=0.001) but lower for the -11377G allele carriers (P=0.017). The significant association with obesity traits was found in the -11391G>A SNP (but not the -11377C>G); the -11391A allele carriers had significantly lower weight (P=0.029), BMI (P=0.019), waist (P=0.003) and hip circumferences (P=0.004) compared to the GG homozygotes. Furthermore, the associations of the -11391G>A with BMI and obesity risk were further modified by monounsaturated fatty acids (MUFA) intake (P-interaction=0.021 and 0.034 for BMI and obesity risk respectively). In subjects with MUFA intake >13% of energy intake (median level), the -11391A carriers had lower BMI (27.1 kg/m2 for GA+AA versus 29.1 kg/m2 for GG, P=0.002) and decreased obesity risk (OR for -11391A = 0.52, 95%CI; 0.28-0.96; P=0.031). No genotype-related differences for BMI or obesity for either allele of -11391A>G in subjects with MUFA intake <13%.