Bollen M, Keppens S, Stalmans W
Department of Biochemistry, Faculty of Medicine, Catholic University of Leven, Belgium.
Diabetologia. 1988 Sep;31(9):711-3. doi: 10.1007/BF00278757.
The activation of glycogen synthase after addition of glucose to isolated hepatocytes became impaired in BB rats after the development of insulin-dependent diabetes. This defect was associated with a decreased hepatic synthase phosphatase activity. Both features correspond closely to previous observations on alloxan-diabetic rats. In contrast, in hyperinsulinaemic db/db mice with a similarly increased plasma glucose concentration (non-insulin-dependent diabetes), the synthase phosphatase activity was essentially normal. We conclude that the decreased hepatic synthase phosphatase activity in insulin-dependent diabetes in rodents is due to the lack of insulin, rather than to the increased intrahepatic glucose concentration.
在分离的肝细胞中加入葡萄糖后，胰岛素依赖型糖尿病发展后的BB大鼠糖原合酶的激活受损。这一缺陷与肝合酶磷酸酶活性降低有关。这两个特征与先前对四氧嘧啶糖尿病大鼠的观察结果密切相符。相比之下，在血浆葡萄糖浓度同样升高的高胰岛素血症db/db小鼠（非胰岛素依赖型糖尿病）中，合酶磷酸酶活性基本正常。我们得出结论，啮齿动物胰岛素依赖型糖尿病中肝合酶磷酸酶活性降低是由于缺乏胰岛素，而非肝内葡萄糖浓度升高。
