Guanghua Zhai1, Meifen Li, Chaowang Zhu. 1. Department of Laboratory Medicine, The North District of Affiliated Suzhou Hospital, Nanjing Medical University, Suzhou, P.R. China.
Abstract
BACKGROUND: Functional studies suggest that the APOA5 -1131T/C polymorphism plays an important role in triglyceride (TG) metabolism, which is an event contributing to the pathogenesis of coronary artery disease (CAD). However, genetic evidence of its effect on CAD is inconsistent. To assess this correlation, we performed a meta-analysis of published data. METHODS: A comprehensive meta-analysis was performed on nine published studies, with a total sample of 2049 subjects and 2373 controls using a fixed effect model. RESULTS: Under the fixed effect model, the risk of the disease was significantly higher in subjects with CC genotype in comparison with both TT (OR: 1.99; 95% CI: 1.64-2.41) and TC (OR: 1.48; 95% CI: 1.22-1.80) subjects. Compared with TT homozygotes, there was 43% increase in the incidence of CAD (OR: 1.43; 95% CI: 1.26-1.61) of C carriers (CC+TC). There was no heterogeneity for these effect estimates. CONCLUSIONS: Our findings support the view that -1131T/C polymorphism of the APOA5 gene is associated with CAD and the C allele might be a genetic risk factor that increases susceptibility to CAD.
BACKGROUND: Functional studies suggest that the APOA5-1131T/C polymorphism plays an important role in triglyceride (TG) metabolism, which is an event contributing to the pathogenesis of coronary artery disease (CAD). However, genetic evidence of its effect on CAD is inconsistent. To assess this correlation, we performed a meta-analysis of published data. METHODS: A comprehensive meta-analysis was performed on nine published studies, with a total sample of 2049 subjects and 2373 controls using a fixed effect model. RESULTS: Under the fixed effect model, the risk of the disease was significantly higher in subjects with CC genotype in comparison with both TT (OR: 1.99; 95% CI: 1.64-2.41) and TC (OR: 1.48; 95% CI: 1.22-1.80) subjects. Compared with TT homozygotes, there was 43% increase in the incidence of CAD (OR: 1.43; 95% CI: 1.26-1.61) of C carriers (CC+TC). There was no heterogeneity for these effect estimates. CONCLUSIONS: Our findings support the view that -1131T/C polymorphism of the APOA5 gene is associated with CAD and the C allele might be a genetic risk factor that increases susceptibility to CAD.