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目的:探讨熊果酸(UA)改善自发性2型糖尿病KKAy小鼠胰岛素抵抗的作用和机制。方法:KKAy小鼠35只,根据随机区组设计方法,分为糖尿病对照组、罗格列酮组、非诺贝特组、熊果酸高剂量组和熊果酸低剂量组,每组7只,以C57BL/6J小鼠作为正常组。药物干预4周,进行一般状态观察,口服糖耐量检测,计算胰岛素抵抗指数(HOMA-IR),采用免疫组化法检测葡萄糖转运体(GLUT4)的表达,并用Westen-blot法进一步检测小鼠肌细胞膜GLUT4蛋白转运情况。结果:与糖尿病对照组相比,熊果酸高剂量组小鼠糖耐量和胰岛素抵抗指数明显改善(P<0.01);熊果酸对小鼠肌细胞GLUT4蛋白表达和转运的影响与对照组比较差异有统计学意义(P<0.01)。结论:熊果酸可有效改善自发性2型糖尿病KKAy小鼠糖耐量和胰岛素抵抗指数,可能是通过提高小鼠肌细胞GLUT4蛋白转运和表达来实现的。
Objective: To investigate the effect and mechanism of ursolic acid (UA) on insulin resistance in spontaneously type 2 diabetic KKAy mice. Methods: Thirty-five KKAy mice were randomly divided into diabetic control group, rosiglitazone group, fenofibrate group, high-dose ursolic acid group and low-dose ursolic acid group Only C57BL / 6J mice were used as normal group. The drug was administered for 4 weeks, and the general state was observed. Oral glucose tolerance test was used to calculate the insulin resistance index (HOMA-IR). The expression of glucose transporter (GLUT4) was detected by immunohistochemistry and further detected by Western blotting Cell membrane GLUT4 protein transport. Results: Compared with the diabetic control group, the high-dose ursolic acid group significantly improved the glucose tolerance and insulin resistance index (P <0.01). The effect of ursolic acid on the GLUT4 protein expression and transport in mouse muscle cells compared with the control group The difference was statistically significant (P <0.01). Conclusion: UA can effectively improve the index of glucose tolerance and insulin resistance in KKAy mice of spontaneous type 2 diabetes mellitus, which may be achieved by enhancing the transport and expression of GLUT4 protein in mouse muscle cells.