肥胖Wistar大鼠骨骼肌细胞GLUT-4转位变化的研究

目的:探讨肥胖大鼠骨骼肌细胞的葡萄糖转运因子4(GLUT-4)转位变化.方法:10周龄雄性Wistar大鼠46只,随机平均分成对照组和肥胖组.6周肥胖模型建立后,用超速蔗糖梯度离心方法分离骨骼肌细胞内膜和外膜的匀浆,用Westem blot方法检测两组大鼠骨骼肌细胞内、外膜GLUT-4的蛋白水平.同时分别检测其空腹血糖、空腹胰岛素和血脂浓度.结果:肥胖组大鼠的胰岛素敏感指数明显下降(P＜0.01),肥胖组的内、外膜GLUT-4蛋白含量均较对照组下降,而且外膜GLUT-4下降比内膜更明显(分别为57.0%、12.2%,P＜0.01).结论:肥胖下调骨骼肌细胞GLUT-4总量,抑制细胞内膜GLUT-4向细胞外膜的转位,提示肥胖大鼠的骨骼肌存在由于GLUT-4下降调节所致的胰岛素抵抗.

Changes in the translocation of GLUT-4 in skeletal muscle cell of rats with obesity

Objective: To investigate the changes in the translocations in the skeletal muscle cell glucose transporter-4 (GLUT-4) in Wistar rats with obesity. Methods: Forty-six male Wistar rats were divided equally and randomly into 2 groups: the experimental group with high fat diet and the control group with normal diet. After 6 weeks, the obese rat model was established. The intracellular and plasma membrane of the skeletal muscle were separated by sucrose gradient ultracentrifugation. The levels of GLUT-4 protein were measured by Western blot analysis, and the levels of the fasting plasma glucose,serum insulin, and serum lipid were also measured. Results: The insulin sensitive index in the experimental group was significantly lower than that in the control group (P<0.01). Compared with the control group, the levels of GLUT-4 protein in intracellular and plasma membrane decreased in the experimental group, and the decrease in plasma membrane was more significant than that in intracellular membrane (decreased by 57% in plasma membranes, and by 12% in intracellular membranes). Conclusion: Obesity inhibits not only the expression but also the translocation of GLUT-4 protein in skeletal muscle cells. The degradation mediation of GLUT-4 may be one of the molecule mechanisms that contribute to the insulin resistance of the skeletal muscle in obese rats.