Lautt W W
Med Hypotheses. 1979 Dec;5(12):1287-96. doi: 10.1016/0306-9877(79)90096-3.
Neural and humoral induction of hepatic glycogenolysis occurs via different pathways. Sympathetic nerve stimulation activates alpha adrenergic receptors to produce what is probably a cyclic AMP independent, Ca++ dependent activation of glycogen phosphorylase. Evidence suggests that phosphorylase 'a' is activated by inhibition of phosphorylase phosphatase and perhaps by activation of phosphorylase kinase. Blood borne catecholamines act via beta adrenergic receptors to produce a cyclic AMP dependent activation of phosphorylase kinase. Additionally, hepatic parasympathetic nerves can produce a dramatic shut-down of hepatic glucose output by activation of glycogen synthetase and inhibition of glycogen phosphorylase. The observed minor effect of insulin or intravenous glucose on hepatic glucose uptake compared to the effect of oral doses of glucose suggests that an additional factor other than insulin can produce hepatic glucose uptake: this factor could be, and probably is, the hepatic parasympathetic nerves. The present hypotheses result from a combination and extrapolation of whole animal physiological and in vitro biochemical data.
肝脏糖原分解的神经和体液诱导通过不同途径发生。交感神经刺激激活α肾上腺素能受体，可能通过一种不依赖环磷酸腺苷（cAMP）、依赖钙离子（Ca++）的方式激活糖原磷酸化酶。有证据表明，磷酸化酶“a”通过抑制磷酸化酶磷酸酶以及可能通过激活磷酸化酶激酶而被激活。血液中的儿茶酚胺通过β肾上腺素能受体发挥作用，产生依赖环磷酸腺苷（cAMP）的磷酸化酶激酶激活。此外，肝脏副交感神经可通过激活糖原合成酶和抑制糖原磷酸化酶，显著减少肝脏葡萄糖输出。与口服葡萄糖的效果相比，观察到胰岛素或静脉注射葡萄糖对肝脏葡萄糖摄取的影响较小，这表明除胰岛素外，还有其他因素可促进肝脏葡萄糖摄取：这个因素可能是，也很可能是肝脏副交感神经。目前的假说来自对全动物生理学和体外生化数据的综合与推断。
