Witters L A, Avruch J
Biochemistry. 1978 Feb 7;17(3):406-10. doi: 10.1021/bi00596a004.
The relative roles of insulin and glucose in the regulation of hepatic glycogen synthase and phosphorylase were studied in hepatocytes from fed rats. Elevation of extra-cellular glucose led to a rapid decrease in phosphorylase a activity followed by a slower increase in glycogen synthase I activity. A reciprocal and coordinate relationship between phosphorylase inactivation and synthase activation in response to glucose was observed; following initial glucose-induced inactivation of phosphorylase, there was a highly significant linear inverse relationship between residual phosphorylase activity and glycogen synthase activation. Insulin led to a further decrease in phosphorylase activity and a 30-50% additional increase in glycogen synthase activity over that caused by glucose. The effects of insulin required the presence of glucose and served to augment acute glucose stimulation of glycogen synthase and inhibition of phosphorylase. Insulin did not perturb the reciprocal and coordinate relationship between phosphorylase inactivation and synthase activation in response to glucose. The results suggest that the ability of insulin to activate hepatic glycogen synthase can be entirely accounted for by its ability to inactivate phosphorylase.
在喂食大鼠的肝细胞中研究了胰岛素和葡萄糖在调节肝糖原合酶和磷酸化酶中的相对作用。细胞外葡萄糖浓度升高导致磷酸化酶a活性迅速下降，随后糖原合酶I活性缓慢增加。观察到磷酸化酶失活与合酶激活之间对葡萄糖的反应存在相互协调的关系；在最初由葡萄糖诱导的磷酸化酶失活后，残余磷酸化酶活性与糖原合酶激活之间存在高度显著的线性负相关。胰岛素导致磷酸化酶活性进一步降低，糖原合酶活性比葡萄糖引起的增加30 - 50%。胰岛素的作用需要葡萄糖的存在，并起到增强糖原合酶对葡萄糖的急性刺激和抑制磷酸化酶的作用。胰岛素并未干扰磷酸化酶失活与合酶激活之间对葡萄糖的相互协调关系。结果表明，胰岛素激活肝糖原合酶的能力完全可以由其使磷酸化酶失活的能力来解释。
