Loweth A C, Scarpello J H, Morgan N G
Department of Biological Sciences, Keele University, Staffordshire, UK.
Biochem Biophys Res Commun. 1996 Jan 17;218(2):423-7. doi: 10.1006/bbrc.1996.0075.
In pancreatic beta-cells, arachidonic acid accumulation results primarily from phospholipid hydrolysis by phospholipase A2, and activation of this enzyme has been shown to accompany glucose-induced insulin secretion. Inhibitors of phospholipase A2 attenuate the secretory response, although the compounds used to date have not discriminated between cytosolic and secretory isoforms of phospholipase A2. In this work, the specific cytosolic phospholipase A2 inhibitor, AACOCF3, caused a dose-dependent inhibition of glucose-induced insulin secretion from isolated rat islets and this response was significantly relieved by exogenous arachidonic acid. The results suggest that, despite the low levels of expression of cytosolic phospholipase A2 in rat islets, this enzyme contributes to the control of glucose-induced insulin secretion in rat pancreatic beta-cells.
在胰腺β细胞中，花生四烯酸的积累主要源于磷脂酶A2对磷脂的水解作用，并且已表明该酶的激活伴随着葡萄糖诱导的胰岛素分泌。磷脂酶A2抑制剂可减弱分泌反应，尽管迄今为止所使用的化合物尚未区分磷脂酶A2的胞质型和分泌型同工酶。在这项研究中，特异性胞质磷脂酶A2抑制剂AACOCF3对分离的大鼠胰岛中葡萄糖诱导的胰岛素分泌产生剂量依赖性抑制作用，并且外源性花生四烯酸可显著缓解这一反应。结果表明，尽管大鼠胰岛中胞质磷脂酶A2的表达水平较低，但该酶在大鼠胰腺β细胞中对葡萄糖诱导的胰岛素分泌控制发挥作用。
