PI3-K对自发性糖尿病大鼠心肌细胞膜GLUT4含量的影响  

Key role of phosphatidylinositol-3-kinase in glucose transporter 4 translocation in cardiomyocytes of spontaneous OLETF rats

作　　者：王东[1] 周丽诺[2] 张伟伟[2] 任惠明[3] 胡仁明[2] 

机构地区：[1]安徽医科大学附属安徽省立医院内分泌科,安徽合肥230001 [2]复旦大学附属华山医院内分泌科,上海200040 [3]复旦大学附属华山医院神经病研究所,上海200040

出　　处：《皖南医学院学报》2008年第6期395-398,共4页Journal of Wannan Medical College

基　　金：国家自然科学基金项目(30270627)

摘　　要：目的:探讨PI3-K在自发性糖尿病大鼠心肌细胞胰岛素抵抗中的作用。方法:①从大鼠心肌组织中抽提纯化总RNA,逆转录合成两组动物的cDNA及cRNA探针,与基因表达谱芯片杂交,扫描并分析统计;②分离培养大鼠心肌细胞,分别加入胰岛素及PI3-K特异性抑制剂LY294002,提取细胞膜蛋白,应用western-blot方法检测心肌细胞膜GLUT4含量的差异。结果:①PI3-K调节亚基基因下调表达达8倍,②胰岛素组应用LY294002后,细胞膜GLUT4表达量仅为抑制前的11.16%。结论:自发性糖尿病大鼠心肌存在胰岛素利用障碍,其关键部位在于PI3-K。Objective：To study the role of pbosphatidylinositol-3-kinase in glucose transporter 4 （GLUT4） translocation in the cardiomyccytes of spontaneous Otsuka Long-Evans Tokushima Fatty（OLETF） rats by incubating with insulin. Methods ： The myocardial tissues at the apex of the rats were obtained for eukaryotic GeneChip analysis. The cardiomyocytes of OLETF rats were isolated by retrograde catheterization in aorta and incubated with insulin and Ly294002, specific inhibitor of phosphatidylinositol-3-kinase （PI3-K）. The myocyte membrane proteins were extracted and western-blot was used to detect the GLUT4 proteins. Results ： PI3-K regulatory subunit gene was found down-regulated by 8 folds in OLETF rats＇ myccardium. Moreover, the LY294002 decreased the insulin-induced GLUT4 translocation for about 88.84%. Conclusion： The impaired utilization of insulin suggests that GLUT4 translocation may depend on a PI3-K pathway in diabetic rats myocardium.

关 键 词：PI3-K 心肌细胞 GLUT4 糖尿病 

分 类 号：R587.1[医药卫生—内分泌]