高血糖削弱鼠脂肪细胞糖的转运及PKB活性

High glucose impaires glucose transport and PKB activity in adipocytes of rats

目的 :探讨高浓度葡萄糖 (高糖 )对原代培养大鼠脂肪细胞的糖转运、蛋白激酶B(PKB)活性及葡萄糖转运子 4 (GLUT4 )的影响。方法 :分离的大鼠脂肪细胞在不同浓度葡萄糖 (5 ,10 ,15 ,2 5mmol·L- 1 )中培养 2 4h ,然后测定糖的转运率 ,并检测细胞内和细胞膜GLUT4蛋白表达、PKB蛋白表达、丝氨酸磷酸化及活性。结果 :高糖使大鼠脂肪细胞的糖摄取率、PKB丝氨酸磷酸化及活性下降 ,而使细胞膜GLUT4表达上调 ;对细胞内PKB和GLUT4蛋白表达无影响。结论 :高糖能诱导胰岛素抵抗 ,其作用机制与影响PKB丝氨酸磷酸化、活性及GLUT4功能等因素有关。

Objective To explore the effect of high glucose on glucose transport activity, protein kinase B (PKB) activity and glucose transporter 4 (GLUT4) in primary cultured rat adipocytes. Methods Isolated rat adipocytes were cultured for 24 h at different glucose concentrations (5, 10, 15 and 25 mmol·L -1 ). The glucose uptake, cellular and membrane GLUT4 expression, PKB protein expression, and PKB serine phosphorylation and activity were measured. Results These adipocytes treated with glucose of different concentrations showed that high glucose impaired glucose uptake, PKB phosphorylaion and activity, and up regulated GLUT4 translocation, but didn't affect protein expression of PKB and GLUT4. Conclusion High glucose can induce insulin resistance; the mechanism may be involved in the effect of high glucose on PKB serine phosphorylation and activity as well as GLUT4 function.