胰岛素促进狗缺血心肌葡萄糖转运子1移位和葡萄糖摄取

Insulin stimulates translocation of glucose transporter 1 and glucose uptake in ischemic myocardium in dogs

观察胰岛素能否刺激缺血心肌葡萄糖转运子 1(GLUT1)移位和葡萄糖摄取。利用自动分析仪测定生理代谢参数 ,应用免疫印迹和免疫荧光法检测GLUT1。胰岛素使缺血心肌细胞质膜GLUT1明显增加 (从 5 2 %± 4%～ 6 7%± 6 % ,P <0 0 5 )。细胞器膜GLUT1则相应减少 ,同时伴随葡萄糖摄取量明显增加 ,是单纯缺血心肌葡萄糖摄取量的 2倍。胰岛素刺激引起GLUT1移位 ,使缺血心肌葡萄糖摄取增加。提示心肌缺血时 。

To investigate if insulin stimulates the translocation of glucose transporter 1(GLUT1) and glucose uptake in ischemic myocardium. Plasma concentrations of glucose, lactate and free fatty acid were determinded by autoanalyser and GLUT1 was studied by immunoblot analysis. Insulin significantly increased sarcolemmic GLUT1 of ischemic myocardium (52%±4% vs 67%±6%, P <0.05) and decreased GLUT1 content in intracellular membrane proportionally. The glucose uptake increased significantly in insulin treated ischemic myocardium. The glucose uptake of insulin treated ischemic myocardium was almost 2 folds greater than that of ischemia alone. Insulin stimulation results in GLUT1 translocation and then increases glucose uptake in ischemic myocardium. These results suggest that insulin facilitates myocardial glucose uptake and utilization during myocardial ischemia.