Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Cardiovasc Diabetol. 2010 Mar 24;9:13. doi: 10.1186/1475-2840-9-13.
Peroxisome proliferator-activated receptor gamma (PPARgamma) is a ligand-activated transcription factor, which regulates gene expression of the key proteins involved in lipid metabolism, vascular inflammation, and proliferation. PPARgamma may contribute to attenuating atherogenesis and postangioplasty restenosis. PPARgamma C161-->T substitution is associated with a reduced risk of coronary artery disease (CAD). Whether or not the gene substitution alters the risk of CAD in type 2 diabetes mellitus (T2DM) patients remains unclear.
A total of 556 unrelated subjects from a Chinese Han population, including 89 healthy subjects, 78 CAD patients, 86 T2DM patients, and 303 CAD combined with T2DM patients, were recruited to enroll in this study. PPARgammaC161-->T gene polymorphism was determined by polymerase chain reaction and restriction fragment length polymorphisms. Plasma levels of lipoproteins, apolipoproteins, glucose, and insulin were measured by ELISA or radioimmunoassay (RIA). The coronary artery lesions were evaluated by coronary angiography.
The frequency of the 161T allele in CAD, T2DM, and CAD combined with T2DM patients was similar to that observed in the healthy control group. However, in CAD combined with T2DM patients, the group with angiographically documented moderate stenoses had a higher frequency of the 161T allele in comparison to the group with severe stenoses (P < 0.05). Moreover, in CAD with T2DM patients, the triglyceride levels and apoB in CC homozygote carriers were significantly higher than those in "T" allele carriers.
PPARgammaC161-->T genotypes weren't significantly associated with the risk of CAD, but were markedly correlated with severity of disease vessels in patients with CAD and T2DM. Furthermore, PPARgammaC161-->T substitution was associated with an altered adipose, but not glucose metabolism. These results indicate that the PPARgamma C161-->T polymorphism may reduce the risk of severe atherogenesis by modulation of adipose metabolism, especially triglycerides and apoB, in Chinese patients with CAD and T2DM.
过氧化物酶体增殖物激活受体γ（PPARγ）是一种配体激活的转录因子，可调节参与脂质代谢、血管炎症和增殖的关键蛋白的基因表达。PPARγ可能有助于减轻动脉粥样硬化形成和血管成形术后再狭窄。PPARγ C161-->T 取代与冠心病（CAD）风险降低相关。该基因取代是否改变 2 型糖尿病（T2DM）患者的 CAD 风险尚不清楚。
本研究共纳入 556 例来自中国汉族人群的无血缘关系个体，包括 89 例健康对照者、78 例 CAD 患者、86 例 T2DM 患者和 303 例 CAD 合并 T2DM 患者。通过聚合酶链反应和限制性片段长度多态性确定 PPARγC161-->T 基因多态性。通过 ELISA 或放射免疫分析（RIA）测量脂蛋白、载脂蛋白、血糖和胰岛素的血浆水平。通过冠状动脉造影评估冠状动脉病变。
CAD、T2DM 和 CAD 合并 T2DM 患者中 161T 等位基因的频率与健康对照组观察到的频率相似。然而，在 CAD 合并 T2DM 患者中，血管造影证实中度狭窄组的 161T 等位基因频率高于严重狭窄组（P<0.05）。此外，在 CAD 合并 T2DM 患者中，CC 纯合子携带者的甘油三酯水平和 apoB 显著高于“T”等位基因携带者。
PPARγC161-->T 基因型与 CAD 风险无显著相关性，但与 CAD 和 T2DM 患者血管病变严重程度显著相关。此外，PPARγC161-->T 取代与脂肪代谢改变相关，而与葡萄糖代谢无关。这些结果表明，在中国 CAD 和 T2DM 患者中，PPARγ C161-->T 多态性可能通过调节脂肪代谢，尤其是甘油三酯和 apoB，降低严重动脉粥样硬化形成的风险。
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