糖尿病大鼠肝脏酶组织化学及胰升糖素受体的研究

STUDIES ON LIVER ENZYME HISTOCHEMISTRY AND GLUCAGON RECEPTOR IN STREPTOZOTOCIN-INDUCED DIABETIC RATS

对链脲佐菌素实验性糖尿病大鼠肝脏酶组织化学及肝细胞膜胰升糖素受体的改变进行了观察,结果显示,糖尿病大鼠肝脏与糖原分解和糖异生作用有关的酶活性均增高;其肝细胞膜胰升糖素受体亲和力与正常大鼠九差异,但糖尿痫大鼠肝细胞膜低亲和力的受体浓度显著高于正常(P<0.05);胰岛素治疗后可使高亲和力受体浓度恢复正常,低亲和力受体浓度降低30.6％。提示胰岛素缺乏时,肝糖异生作用增强是肝糖输出增加的重要原因之一;肝细胞膜胰升糖素受体增加可能是其升血糖效应增强的细胞基础;胰岛素可能直接或间接地调节着肝细胞胰升糖素受体的数量。

Changes of liver enzyme histochemistry and characteristics of glucagon receptor on liver cell plasma membrane were observed in streptozotocin-induced diabetic rats. The results showed that glycogenolytic and glyconeogenetic enzyme activities of liver were increased in diabetic rats and were higher than those of normal rats. There were no marked differences concerning both low and high affinities of glucagon receptors between normal and diabetic rats, but the concentration of low affinity glucagon receptor was significantly higher for diabetic rats than for normal rats. Compared with untreated diabetic rats, the concentration of high affinity glucagon receptor was normalized and that of low affinity receptor decreased by 30. 6% in insulin-treated diabetic rats. The present study implies that: 1)DURING insulin deficiency the increase in liver glyconeogenesis may be one of the important factors to induce increment of liver glucose output; 2) the increase in glucagon receptor binding to liver in streptozotocin-induced diabetic rats may provide a cellular basis for the increased glycemic and ketonemic response to glucagon in insulin-deprived diabetics; 3) since in diabetic rats insulin treatment results in a reversal of increased glucagon binding, it is possible that insulin regulates the glucagon receptor either directly or through its effect on the plasma glucagon concentration.