摘要
目的：为了探索烧伤后胰岛素受体信号传递缺陷的机理，以阐明烧伤胰岛素抵抗的分子基础。方法：采用ＷＧＡ－Ｓｅｐｈａｒｏｓｅ４Ｂ亲和层杆纯化大鼠肝脏和肌肉细胞膜胰岛素受体，通过胰岛素受体蛋白γ－３２Ｐ磷酸化的ＳＤＳ－ＰＡＧＥ放射自显影和外源底物磷酸化，观察烫伤大鼠早期胰岛素受体β－亚基自身磷酸化和受体酪氨酸蛋白激酶（ＩＲ－ＴＰＫ）活性变化。结果：３０％ＴＢＳＡⅢ°烫伤３ｄ大鼠肝和肌肉胰岛素受体β－亚基自身磷酸化能力明显下降；胰岛素受体ＴＰＫ活性亦明显降低并对胰岛素刺激的反应性明显减退。结论：胰岛素受体信号偶联障碍可能是烧（创）伤后胰岛素抵抗发生的分子基础。
Objective: To clarify the mechanism and molecular basis of insulin resistance after severe scalding. Methods: In the rats inflicted with 30% TBSA scalding, the insulin receptors on the cell membrane of the liver and skeletal muscle were partially purified with WGA Sepharose 4B affinity chromatography and then the changes of autophosphorylation of insulin receptor β subunit and the activity of tyrosine protein kinase insulin receptors (TR TPR) were observed with SDS PAGE autoradiography of phsophorylation of insulin receptors and phosphorylation of exogenous substrate. Results: The degree of autophospholation of insulin receptor β subunit and the activity of IR TPR and its sensitivity to insulin stimulation in the liver and skeletal muscle were markedly decreased as compared with the control. Conclusion: The defect of insulin receptor signal transduction may be the molecular mechanism of insulin resistance after thermal injury.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1997年第1期4-6,共3页
Journal of Third Military Medical University
基金
国家自然科学基金
关键词
胰岛素
烧伤
信号传导缺陷
burns
receptor
insulin
tyrosine protein kinase
