阿片肽对分离的肝细胞中糖原分解的刺激作用。
The stimulation of glycogenolysis in isolated hepatocytes by opioid peptides.
作者信息
Leach R P, Titheradge M A
出版信息
Biochem J. 1986 Sep 1;238(2):531-5. doi: 10.1042/bj2380531.
The opioid peptides [Leu]enkephalin and dynorphin-(1-13) were shown to enhance glycogen breakdown when added directly to hepatocytes. This was the result of a concerted effect on the enzymes of glycogen metabolism, with a stimulation of glycogen phosphorylase activity and a simultaneous decrease in glycogen synthase I activity. The latter only became significant when the enzyme was activated by incubating the cells in presence of 20 mM- or 40 mM-glucose. The effect of the opioid peptides was independent of an increase in cyclic AMP or any change in the activity ratio of the cyclic AMP-dependent protein kinase and was abolished by depleting the cells of Ca2+. Both [Leu]enkephalin and dynorphin-(1-13) produced a significant decrease in cyclic AMP formation, suggesting that in liver, as in neuronal tissue, they may act by inhibiting adenylate cyclase activity.
阿片肽亮氨酸脑啡肽和强啡肽 -（1 - 13）直接添加到肝细胞中时，可增强糖原分解。这是对糖原代谢酶协同作用的结果，刺激了糖原磷酸化酶活性，同时糖原合酶I活性降低。只有当细胞在20 mM或40 mM葡萄糖存在下孵育激活该酶时，后者才变得显著。阿片肽的作用与环磷酸腺苷（cAMP）增加或环磷酸腺苷依赖性蛋白激酶活性比值的任何变化无关，并且通过耗尽细胞内的Ca2 +而消除。亮氨酸脑啡肽和强啡肽 -（1 - 13）均使环磷酸腺苷形成显著减少，表明在肝脏中，与神经组织一样，它们可能通过抑制腺苷酸环化酶活性起作用。
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