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目的:初步研究钙超载后心肌细胞胰岛素抵抗与葡萄糖转运蛋白4(GLUT4)活性之间的关系,探讨钙超载后心肌细胞胰岛素抵抗的分子机制。方法:采用伊屋诺霉素构建不同程度成年大鼠心肌细胞钙超载模型;应用同位素示踪技术观察胰岛素刺激大鼠心肌细胞的葡萄糖摄取效应,用West-ern blot分析检测胰岛素刺激的心肌细胞膜GLUT4的活性变化。结果:钙超载后心肌细胞表现出严重的胰岛素抵抗,实验组(1.0μmol/L伊屋诺霉素)心肌细胞膜基础GLUT4磷酸化形式和对照组无统计学差异,但胰岛素刺激的GLUT4磷酸化形式显著增加,为对照组的226.3%(P<0.05)。结论:胰岛素刺激的GLUT4活性障碍是心肌细胞钙超载后胰岛素抵抗的另一重要分子机制;缺血再灌注心肌细胞内钙超载是急性胰岛素抵抗的始动因素。
OBJECTIVE: To study the relationship between insulin resistance and glucose transporter 4 (GLUT4) activity in cardiomyocytes after calcium overload and to explore the molecular mechanism of insulin resistance in cardiomyocytes after calcium overload. Methods: Calcium overload model of cardiomyocytes was established by ionomycin. The effects of insulin on myocardial glucose uptake were observed by isotope labeling. The expression of GLUT4 in insulin-stimulated myocardium was detected by West-ern blot. Activity changes. RESULTS: Cardiac myocytes showed severe insulin resistance after calcium overload. There was no significant difference in basal GLUT4 phosphorylation between the experimental group (1.0 μmol / L ionomycin) and the control group, but insulin-stimulated GLUT4 phosphorylation Significantly increased to 226.3% of the control group (P <0.05). CONCLUSION: Insulin-stimulated GLUT4 activity disorder is another important molecular mechanism of cardiomyocyte calcium overload. Insulin-stimulated calcium overload is the initiating factor of acute insulin resistance.