| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Research Abstract |
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.
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