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目的研究胰岛素降解酶(IDE)活性变化与胰岛素抵抗(IR)发生、发展之间的关系。方法以目前公认的IR细胞模型-高浓度胰岛素诱导培养的原代大鼠肝细胞为研究对象,检测细胞的IDE活性和反映细胞胰岛素敏感性的14C-2-脱氧葡萄糖掺入率及14C-醋酸盐掺入率,并观察IDE活性增强剂碘乙酰胺和IDE活性抑制剂氯喹对上述指标的影响。结果IR细胞模型IDE活性显著高于对照细胞,两种掺入率显著低于对照细胞,而且IR细胞模型IDE活性与两种掺入率呈显著负相关关系。此外,碘乙酰胺可显著提高IR细胞模型IDE活性,但显著降低其两种掺入率;氯喹的作用则与其刚好相反。结论IDE活性异常升高可能是引起大鼠肝细胞胰岛素敏感性下降的原因之一;胰岛素降解抑制剂氯喹可能通过抑制胰岛素降解过快所致的IR,从而改善机体的胰岛素敏感性。
Objective To study the relationship between the changes of insulin activity (IDE) and the occurrence and development of insulin resistance (IR). Methods The primary cultured rat hepatocytes induced by high concentration of insulin, the currently accepted IR cell model, were used as experimental subjects. The activity of IDE and the incorporation rate of 14C-2-deoxyglucose and 14C-2-DE Acid addition rate, and observe the IDE activity enhancers iodoacetamide and IDE activity inhibitor chloroquine on the above indicators. RESULTS: The IDE activity of IR cell model was significantly higher than that of control cells, and the incorporation rate of two kinds of IR cells was significantly lower than that of control cells. There was a significant negative correlation between the IDE activity and the incorporation rate of IR cells. In addition, iodoacetamide significantly increased IDE activity in IR cell models, but significantly reduced both incorporation rates; chloroquine had the opposite effect. Conclusions The abnormal elevation of IDE activity may be one of the reasons for the decrease of insulin sensitivity in rat hepatocytes. Chloroquine, an inhibitor of insulin degradation, may improve the body’s insulin sensitivity by inhibiting the IR induced by insulin degradation.