Best L, Malaisse W J
Biochim Biophys Acta. 1983 Jan 7;750(1):157-63. doi: 10.1016/0005-2760(83)90215-1.
Carbamylcholine produced a concentration-dependent stimulation of labelling of phosphatidylinositol and phosphatidic acid in rat islets of Langerhans following preincubation with 32PO43(-). The time course of these effects suggested that the initial action of carbamylcholine was to stimulate phosphatidic acid production, presumably by causing hydrolysis of phosphatidylinositol. This conclusion was substantiated by experiments in which islet phospholipids were pre-labelled with [3H]arachidonic acid. Under these conditions, carbamylcholine caused a loss of radioactivity from phosphatidylinositol, together with an increase in labelling of phosphatidic acid. The effects of carbamylcholine on islet phospholipid labelling were not dependent upon the presence of added Ca2+, but were abolished by EDTA and by atropine. An apparent stimulation of phosphatidylinositol and phosphatidic acid metabolism was also induced by cholecystokinin-pancreozymin, whereas glucagon, arginine, glibenclamide and thyrotropin had no significant effect. The data suggest that enhanced activity of the so-called phosphatidylinositol cycle may be an important event in regulating secretory activity of islets in response to certain neurotransmitter and hormonal stimuli. Furthermore, the results are compatible with the hypothesis that increased phospholipid metabolism may play a role in the modulation of ionic fluxes during stimulation by such agents.
在用32PO43(-)预孵育后，氨甲酰胆碱对大鼠胰岛中磷脂酰肌醇和磷脂酸的标记产生浓度依赖性刺激。这些效应的时间进程表明，氨甲酰胆碱的初始作用是刺激磷脂酸的产生，推测是通过引起磷脂酰肌醇的水解。用[3H]花生四烯酸预标记胰岛磷脂的实验证实了这一结论。在这些条件下，氨甲酰胆碱导致磷脂酰肌醇的放射性丧失，同时磷脂酸的标记增加。氨甲酰胆碱对胰岛磷脂标记的影响不依赖于添加的Ca2+的存在，但被EDTA和阿托品消除。胆囊收缩素-促胰酶素也诱导了磷脂酰肌醇和磷脂酸代谢的明显刺激，而胰高血糖素、精氨酸、格列本脲和促甲状腺素没有显著影响。数据表明，所谓的磷脂酰肌醇循环活性增强可能是胰岛在响应某些神经递质和激素刺激时调节分泌活性的一个重要事件。此外，结果与以下假设一致，即磷脂代谢增加可能在这类物质刺激期间离子通量的调节中起作用。
