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01.10.2012 | review article | Ausgabe 19-20/2012

Wiener klinische Wochenschrift 19-20/2012

The meta-analysis of the association of PPARG P12A, C161T polymorphism and coronary heart disease

Wiener klinische Wochenschrift > Ausgabe 19-20/2012
Saidan Ding, Leping Liu, Qǐ-Chuan Zhuge, Zhen Yu, Xing Zhang, Jieya Xie, Weilong Hong, Silu Wang, Yunxiu Yang, MD Bicheng Chen



Two common variations of peroxisome proliferator-activated receptor γ (PPARG), P12A (Pro12Ala, rs1801282), and C161T (His447His, rs3856806), are thought to have an effect on susceptibility to coronary heart disease (CHD), but the results are inconsistent. Therefore, a meta-analysis of published studies was performed.


The electronic databases, PubMed, Embase, Web of Science, and CNKI (China National Knowledge Infrastructure) were searched for studies to include in the present meta-analysis (last search was updated on 30 Aug. 2011). Twenty studies testing the association between PPARG gene polymorphisms and CHD were examined: 12 studies of P12A; 8 studies of C161T. Overall and ethnicity-specific summary odds ratios and corresponding 95 % confidence intervals for CHD associated with these polymorphisms were estimated using fixed- and random-effects models. Heterogeneity and publication bias were evaluated. A total of 20 studies including 5,795 cases and 9,069 controls were included in this meta-analysis.


No significant associations were found in carriers of the rare Ala allele of the P12A polymorphism versus the common Pro/Pro genotype among the studies with both of the fixed-effect and random-effect model. In the subgroup analyses by ethnicity, source of control and type of study, no significant risks were found. For PPARG C161T, carriers of the T variant of C161T polymorphism were associated with an increased risk of CHD (OR = 1.182, 95 % CI: 1.023–1.341, Pheterogeneity = 0.002), and in the stratified analysis by ethnicity and source of controls, the contrast of CT + TT vs. CC all produced significant association in Asian and hospital-based controls (OR = 1.276, 95 % CI: 1.084–1.468, Pheterogeneity = 0.055; OR = 1.164, 95 % CI: 1.001–1.326, Pheterogeneity = 0.002),when the fixed-effect model was used. But they were all insignificant with the random-effect model.


This meta-analysis suggests that the PPARG C161T polymorphism marginally contributes to increased susceptibility to CHD and marginally increased association between PPARG H477H polymorphism and CHD also appeared in Asian and hospital-based controls. But PPARG P12A polymorphism is not associated with CHD risk.

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