糖皮质激素诱导胰岛素信号肽磷酸化的改变及功能下降  

GLUCOCORTICOID-INDUCED CHANGE OF INSULIN SIGNALING PEPTIDES PHOSPHORYLATION AND DECREAS THEIR FUNCTION

作　　者：刘慧霞[1] 

机构地区：[1]中南大学湘雅医院内科,长沙410008

出　　处：《中国现代医学杂志》2001年第8期51-52,共2页China Journal of Modern Medicine

摘　　要：目的 :探讨糖皮质激素诱导胰岛素抵抗的分子机理。方法 :分离的老鼠脂肪细胞在 5mM浓度的糖加地塞米松 (Dex) (0 .3uM)孵育 2 4h ,然后测定糖的转运活动、细胞内胰岛素受体 β亚单位、胰岛素受体底物及PKB磷酸化 ;PKB、GLUTI、GLUT4的蛋白表达以及GLUT4的易位。结果 :Dex抑制了糖的转运活动、细胞内PKB、GLUTI的蛋白表达 ,对GLUT4的量无影响 ,但明显削弱了它从包内易位至包膜 ;Dex还明显下降了胰岛素受体底物和PKB的磷酸化。结论 :糖皮质激素可以诱导胰岛素抵抗。其机理可能与影响了细胞内胰岛素信号肽磷酸化。Objective:To explore the molecular mechanism of glucocorticoid-induced insulin resistance.Methods:Isolated rat adipocytes were cultured for 24h at 5mM glucose with dexamethasone(0.3μM).Then the glucose uptake,cellular content of insulin signaling peptides(PKB,GLUT1,GLUT4)as well as their phosphorylation were measured.Results:Dex have shown to impair glucose uptake,the cellular PKB,GLUT1 protein expression,IRSs and PKB phosphorylaiton as well as GLUT4 translocation.Conclusions:glucocorticoid can induce insulin resistance.The mechanism may be multiple defects:at the level of insulin signaling peptides expression,phosphorylation as well as GLUT4 translocation.

关 键 词：胰岛素抵抗 Western BLOT PKB GLUTLI GLUT4 磷酸化 

分 类 号：R587.1[医药卫生—内分泌]