摘要
以３０％体表面积背部皮肤全层烫伤大鼠为模型，通过建立肝细胞膜和骨骼肌细胞膜外源性底物磷酸化的分析方法，观察烫伤后３ｄ胰岛素刺激的胰岛素受体酪氨酸蛋白激酶活性的改变，探讨创伤后胰岛素抵抗的分子机理；结果表明：烫伤早期大鼠表现胰岛素抵抗，肝细胞和骨骼肌细胞膜刺激外源性底物磷酸化的基础值增高而胰岛素刺激胰岛素受体酪氨酸蛋白激酶的反应能力则明显减退。提示烫伤后胰岛素受体酪氨酸蛋白激酶对胰岛素刺激的反应性的降低，可能影响了胰岛素受体信号的传导，从而引起由酪氨酸蛋白激酶介导的胰岛素刺激的葡萄糖跨膜转运和糖原合成等信号偶联通路发生障碍导致胰岛素抵抗。
After the rats were inflicted with 30%TBSA full thickness scalding on the back,the changes of insulin receptor tyrosine protein kinase(IRTPK)were studied on the 3rd day postscalding with the phosphorylation of external substrates stimulated with hepatic and muscular cytomembranes to determine the possible molecular mechanism of insulin resistance after scalding.It was found that insulin resistance appeared in the early stage postscalding while the basic value of the phosphorylation of external substrates stimulated with hepatic and muscular cytomembrane was increased and the activity of IRTPK to insulin was greatly suppressed as compared with the control.These facts indicate that the imparied responses of IRTPK to the stimulation of insulin may affect down-stream signal transmission of the insulin receptors and then the signal coupling pathway for the glucose transmembranous transportation and glycogen synthesis mediated with IRTPK and stimulated with insulin is obstructed.Consequently,insulin resistance occurs.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1996年第1期1-4,共4页
Journal of Third Military Medical University
基金
国家自然科学基金
关键词
灼伤
胰岛素
酪氨酸
蛋白激酶
胰岛素抵抗
scalding
insulin receptor
tyrosine protein kinase
insulin resistance
rat
