骨骼肌细胞膜去极化对葡萄糖转运子4转位的调节作用  

Mechanism of the depolarization-regulated glucose transporter 4 translocation in skeletal muscle cells

作　　者：刘琳娟[1] 姚智[1] 牛文彦[1] 

机构地区：[1]天津医科大学免疫学教研室,天津300070

出　　处：《天津医科大学学报》2009年第2期163-165,175,共4页Journal of Tianjin Medical University

基　　金：国家自然科学基金资助项目(30570912;30670802);国家自然科学基金委员会-加拿大卫生研究院健康研究合作项目(30611120532);天津市应用基础研究重点项目(07JCZDJC07900)

摘　　要：目的:探讨高钾造成的骨骼肌细胞膜去极化对葡萄糖转运因子4(GLUT4)转位的调节作用。方法:用55 mmol/L的葡萄糖酸钾孵育L6GLUT4myc肌管使细胞膜去极化,用偶联抗体的比色法检测细胞膜上GLUT4的数量。结果:膜去极化介导的GLUT4myc转位呈时间依赖性,2 min和5 min时细胞膜上GLUT4myc的含量显著高于基础组(P<0.05),并随时间的延长回复到基础状态;去极化作用同样急性增加钙/钙调蛋白依赖性蛋白激酶II的磷酸化。结论:高钾诱导的细胞膜去极化可使膜表面GLUT4myc快速增加,钙/钙调蛋白依赖性蛋白激酶II可能参与高钾刺激的骨骼肌细胞GLUT4myc转位的机制。Objective： To study the effect of cell membrane depolarization on glucose transporter 4 （GLUT4） translocation in skeletal muscle cells. Methods： L6GLUT4myc cells were depolarized by incubating with 55mmol/L potassium gluconate. The amount of GLUT4myc on the cell surface was measured by an antibody-coupled colorimetric absorbance assay. Results： That membrane depolarization induced GLUT4rnyc translocation was time dependent. The amounts of ceil surface GLUT4myc were significant higher than basal at 2 minutes and 5 minutes （P〈0.05, respectively） and back to basal in 10 minutes. Depolarization also acutely stimulated phosphorylation of calcium/ealmodulin-dependent protine kinase Ⅱ （CaMK Ⅱ） in 2 minutes. Conclusion： Membrane depolarization induced by high potassium quickly increases cell surface GLUT4 and CaMK Ⅱ phosphorylation. CaMK Ⅱ may involve in the mechanism of high potassium-stimulated GLUT4myc translocation in muscle cells.

关 键 词：骨骼肌 去极化 葡萄糖转运因子4 L6GLUT4myc 转位 

分 类 号：R392.11[医药卫生—免疫学]