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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。
The streptozotocin experimental diabetic rats liver enzymatic histochemistry and hepatocyte membrane glucagon receptor changes were observed, the results showed that the liver of diabetic rats and glycogenolysis and gluconeogenesis related enzyme activity The affinity of hepatic cell membrane glucagon receptor was similar to that of normal rats, but the receptor of hepatocyte membrane hyponatremia in diabetic rats was significantly higher than that in normal rats (P <0.05). After insulin treatment, high affinity Receptor concentration returned to normal, low affinity receptor concentration decreased 30.6%. Prompted insulin deficiency, increased hepatic gluconeogenesis is an important reason for increased hepatic glucose output; increased hepatic cell membrane glucagon receptor may be its cellular basis for increased blood glucose effect; insulin may be directly or indirectly regulate Hepatocyte glucagon receptor number.