Association of ADIPOQ gene polymorphisms and coronary artery disease risk: A meta-analysis based on 12 465 subjects

Introduction: Coronary artery disease (CAD) is one of the most common cardiovascular diseases and is a major cause of morbidity and mortality worldwide. Various researchers have investigated the role of ADIPOQ gene in the risk of CAD, yet their results have been inconsistent. Methods: To evaluate the association between ADIPOQ genetic polymorphisms and CAD risk, relevant studies published before October 2011 were identified by searching PubMed and EMBASE. Studies were selected using previously defined criteria. The strength of the relationship between the four single nucleotide polymorphisms (SNPs) of the ADIPOQ gene and CAD risk was assessed using odds ratios (ORs). Results: A total of 12 465 subjects from 17 case-control studies were identified in the present study. Based on the relevant studies, it was determined that the risk of CAD was not associated with rs2241766 in any genetic model. Increased risk of CAD was associated with rs266729 in allele contrast (1.11, [1.03, 1.20]) and dominant genetic model (1.15, 95% CI: [1.05, 1.27]); increased risk of CAD was also associated with rs822395 in additive (1.63, 95% CI: [1.19, 2.22]) and recessive genetic model (1.71, 95% CI: [1.27, 2.30]). It was further determined that the rs1501299 polymorphism reduced the risk of CAD in the additive (0.80, 95% CI: [0.67, 0.94]) and recessive genetic model (0.81, 95% CI: [0.68, 0.95]). In the stratified analysis, significant associations were found in Asian subjects for rs266729 and in Caucasian subjects for rs1501299. Conclusion: There is an association between ADIPOQ gene polymorphisms and CAD risk. Different SNPs of the ADIPOQ gene have different associations with CAD risk, and appear to increase risk in individuals of Asian ethnicity while decrease the CAD risk in Caucasians. However, the overall strength of association was mild to moderate. Crown Copyright (C) 2012 Published by Elsevier Ltd. All rights reserved.