The analysis of the function of PPARγin endothelium on the attenuation of the diabetic vascular disease using PPARγendothelium specific deficient mice.

合成的PPARγ配体为改善与脂肪细胞分化相关的胰岛素抵抗提供了证据。合成的PPARγ配体对血管系统的有效作用已有报道，但其机制尚不清楚。为研究血管内皮细胞表达的PPARγ在糖尿病血管病变过程中的作用，对内皮细胞特异性PPARγ进行了敲除(PPARγ)。E-Null)小鼠。PPARγ.与对照PPARγ相比，喂食高脂饲料的E基因缺失小鼠的收缩压显著升高。E野鼠。经高脂饮食治疗后，PPARγ大鼠主动脉中Egr-1、IL-1、IL-6的表达水平明显升高。与PPARγ相比，E基因缺失的小鼠显著升高。E野鼠。PPARγ.饲喂高脂饲料的E基因缺失小鼠血糖升高得到改善，肝脏脂肪蓄积减少，而PPARγ基因缺失。与PPARγ相比，E基因缺失的小鼠表现出更高的血清甘油三酯浓度和游离脂肪水平。E野鼠。PPARγ.高脂饲料喂养的E-Null和ApoE基因敲除小鼠动脉粥样硬化形成速度加快，但动脉粥样硬化区的发生率与PPAR-γ无显著差异。E-空-APOE KO和PPARγ。野生-APOE KO小鼠。本研究证明，在apoE基因敲除小鼠中，内皮细胞表达的PPARγ具有调节炎症和脂代谢的作用，而表达于内皮细胞的PPARγ对动脉粥样硬化的进展无明显影响。

The synthetic PPARγligands have provided the evidence with the improvement of insulin resistance associated with adipocyte differentiation. The effective role of synthetic PPARγligands on vascular system has been reported, but the mechanism has not been clear. To study the role of PPARγexpressed in endothelial cell on the process of diabetic vascular disease, the endothelial cell specific PPARγknock out(PPARγ. E-null) mice were produced. PPARγ. E-null mice fed with high fat diet had significantly elevated systolic blood pressure compared with control PPARγ. E-wild mice. After high fat diet treatment the expression levels of Egr-1, IL-1βand IL-6 in the aorta of PPARγ. E-null mice were elevated compared with PPARγ. E-wild mice. PPARγ. E-null mice fed high fat diet showed the improvement of elevated glucose level and fewer fat accumulation in liver whereas PPARγ. E-null mice showed higher concentration of serum triglyceride and free fatty lipid levels compared with PPARγ. E-wild mice. PPARγ. E-null crossed with apoe knock out mice fed with high fat diet showed accelerated atherogenesis, but there was no significant difference in the rate of atherosclerotic region in aorta between PPARγ. E-null-apoe KO and PPARγ. wild-apoe KO mice. In this study it is proved that PPARγexpressed in endothelial cell regulates inflammation and lipid metabolism whereas PPARγexpressed in endothelial cell has no significant effect on the progression of atherogenesis in apoe knock out mice.