Strickland W G, Blackmore P F, Exton J H
Diabetes. 1980 Aug;29(8):617-22. doi: 10.2337/diab.29.8.617.
The effects of epinephrine, vasopressin, and A23187 on glycogen synthase and phosphorylase were examined in isolated rat liver parenchymal cells from fed animals. In normal calcium-containing hepatocytes, epinephrine, vasopressin, and A23187 were more potent at inactivating glycogen synthase, previously activated with 30 mM glucose, than at activating phosphorylase. In calcium-depleted hepatocytes (cells washed and incubated with 1 mM EGTA), the effect of epinephrine on both enzyme activities was impaired, while the effects of vasopressin and A23187 were completely abolished. Insulin was more effective at inhibiting the effects of epinephrine in calcium-depleted cells, but it was without effect on vasopressin and A23187 actions. The ability of epinephrine, vasopressin, and A23187 to elicit calcium efflux from cells was not altered by the presence of 30 mM glucose. These findings are consistent with the idea that the alpha-adrenergic inactivation of liver glycogen synthase may be a result of the increased stimulation of a calcium-dependent protein kinase, possibly phosphorylase b kinase.
在取自喂食动物的离体大鼠肝脏实质细胞中，研究了肾上腺素、血管加压素和A23187对糖原合酶和磷酸化酶的作用。在正常含钙的肝细胞中，肾上腺素、血管加压素和A23187对先前用30 mM葡萄糖激活的糖原合酶的失活作用，比激活磷酸化酶的作用更强。在缺钙的肝细胞（用1 mM乙二醇双四乙酸洗涤并孵育的细胞）中，肾上腺素对两种酶活性的作用受损，而血管加压素和A23187的作用则完全消失。胰岛素在抑制缺钙细胞中肾上腺素的作用方面更有效，但对血管加压素和A23187的作用没有影响。30 mM葡萄糖的存在并未改变肾上腺素、血管加压素和A23187从细胞中引发钙外流的能力。这些发现与以下观点一致，即肝糖原合酶的α-肾上腺素能失活可能是钙依赖性蛋白激酶（可能是磷酸化酶b激酶）刺激增加的结果。
