以离体和在体脂肪细胞为模型，查明在过氧化物酶增殖体激活受体ｇａｍｍａ（ＰＰＡＲＹ）的配体作用下，Ｏｘ－ＬＤＬ诱导的脂肪细胞核激素受体ＰＰＡＲＹ和膜表面受体ＣＤ３６表达的情况及其与脂肪细胞摄取Ｏｘ－ＬＤＬ能力的关系，以探索Ｏｘ－ＬＤＬ体内代谢的新途径，丰富脂蛋白氧化学说，并为胰岛素增敏剂防治动脉粥样硬化提供实验依据。

Coronary heart disease is a multi-factorial disease. In most cases, risk is determined by a synergy between two or more risk factors, each often of only mild degree. Peroxisome Proliferator-Activated Receptors (PPAR) as a nuclear receptor and transcription factor involves in regulation of many target gene and plays an important role in lipid metabolism, insulin sensitivity, obesity, inflammation and atherosclerosis. PPARg mainly locates in adipocytes and also is expressed in monocytes and macrophages. PPARg not only modulates the differentiation of adipocytes but also involves in the fomation of foam cell.. Reverse transcript polymerase chain reaction and polymerase chain reaction-restricted fragments length polymorphism were used to determine the expression and genotype of PPARg. PPARγCT genotype frequency was significantly lower in the coronary heart disease patients than in healthy controls. A significant interaction between apoE ε4 genotype and PPARγC161?T variants was detected with respect to the effect on coronary heart disease. PPARγ may involve in the process of acute coronary syndrom. We observed that subcutaneous adipocytes could uptake Ox-LDL , the ability of adipocytes to uptake Ox-LDL was decreased in rabbits with hypercholesterolemia. Additionally , PPARγactivator partially restored the Ox-LDL uptake in adipocytes of hypercholesterolemic rabbits, which can be explained by the mRNA upregulation of PPAR and CD36 expressions. .This finding strongly indicate that adipocyte may be another pathway for Ox-LDL metabolism in vivo. The impaired of Ox-LDL uptake in adipocytes may play potential role on the progression of atheroslcerosis. Therefore, PPAR activator could improve the Ox-LDL uptake in adipcoytes, which provide new insighting for the prevention of atherosclerosis..