熊果酸通过葡萄糖转运体改善KKAy小鼠胰岛素抵抗的机制  

Mechanism of Ursolic acid in ameliorating KKAy mice insulin resistance via GLUT4

作　　者：王冠梁[1] 李迪[2] 王琳[2] 刘甲寒[2] 朱德增[2] 

机构地区：[1]中国人民解放军第60医院肿瘤科,大理671003 [2]第二军医大学附属上海长海医院中医科,上海200433

出　　处：《中华中医药杂志》2013年第3期787-790,共4页China Journal of Traditional Chinese Medicine and Pharmacy

基　　金：国家自然科学基金项目(No.81073116)~~

摘　　要：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 explore the effects and mechanism of Ursolic acid（UA） improving insulin resistance in spontaneous type 2 diabetes, the KKAy mice. Methods： 35 KKAy mice were divided into 5 groups according to randomized block design, which were control group, rosiglitazone group, fenoflbrate group, UA high-dose group and UA low-dose group respectively, with C57BL/6J mice as normal control group, 7 mice per group. In the meantime, the influence of mice ordinary condition, oral glucose tolerance test（OGTT） and HOMA-IR was detested. At the end of the 4th week, the protein expression of glucose transporter 4（GLUT4） and the transport situation were detected by immunohistochemisty method and western blot respectively. Results： After 4 weeks intervention, OGTT and HOMA-IR in high dose Ursolic acid group have changed, showing statistically significant differences compared to DM control group（P〈0.01）; high dose Ursolic acid has depressant effect on the GLUT4 protein expression and transshipment（P〈0.01）. Conclusion： The effects of UA in improving spontaneous T2DM KKAy mice insulin resistance might be closely related with affecting content of GLUT4 and regulating the transshipment of GLUT4.

关 键 词：熊果酸 胰岛素抵抗 罗格列酮 非诺贝特 葡萄糖转运蛋白4 

分 类 号：R587.1[医药卫生—内分泌]