高胰岛素血症加重高糖对PKB丝氨酸磷酸化的抑制作用  

HIGH INSULIN AMPLIFY HIGH GLUCOSE-INDUCED INHIBITION OF PKB SERINE PHOSPHORYLATION

作　　者：刘慧霞[1] 

机构地区：[1]中南大学湘雅医院内分泌科,长沙410008

出　　处：《中国现代医学杂志》2002年第9期38-40,共3页China Journal of Modern Medicine

摘　　要：目的 :探讨高胰岛素和高浓度糖 (高糖 )共同作用对原代培养老鼠脂肪细胞的蛋白激酶B(PKB)丝氨酸磷酸化及葡萄糖转运子 4(Glut4)的影响。方法 :分离的老鼠脂肪细胞在 5、2 5mM糖或加胰岛素 10 4 μU/ml培养基中孵育 2 4h ,然后测定糖的转运率、细胞内和细胞膜Glut4及PKB蛋白表达、PKB丝氨酸磷酸化。结果 :高糖抑制了这些细胞的糖摄取率、PKB丝氨酸磷酸化 ,高胰岛素加重高糖的以上抑制作用 ;高糖增加细胞膜的蛋白表达 ,而高胰岛素对抗高糖的此作用。结论 :高糖能诱导胰岛素抵抗 ,高胰岛素加重高糖的此作用 ,其作用机制与影响PKB丝氨酸磷酸化及Glut4易位等因素有关。Objective:To explore the effects of high insulin and high glucose on PKB serine phosphorylation and glucose transporter 4 (Glut4) translocation. Methods:Isolated primary cultured rat adipocytes were cultured for 24 hours at 5 or 25 mM glucose with or without insulin(10 4μU/ml).Then the glucose uptake, the protein expression of Glut4 and PKB as well as PKB serine phosphorylation were measured. Results:Twenty-five mM glucose impaired glucose uptake and PKB phosphorylation. Combined insulin and high glucose amplified the above suppression. High glucose increased plasma membrance Glut4 content, high insulin abolished its effect. The total cellular Glut 4 was unaffected. Conclusions:High glucose can induce insulin resistance, high insulin can amplify the effect. The mechanism may be involved in affecting PKB serine phosphorylation and Glut4 translocation.

关 键 词：高血糖 胰岛素抵抗 受体 胰岛素 葡萄糖转运子4 磷酸化 

分 类 号：R587[医药卫生—内分泌]