脂氧合酶依赖性胰岛素释放的重新诠释：花生四烯酸的哪些代谢产物，还是根本没有？

A re-interpretation of lipoxygenase-dependent insulin release: which metabolites of arachidonic acid, or none?

作者信息

Metz S A

出版信息

Life Sci. 1986 Jun 9;38(23):2069-76. doi: 10.1016/0024-3205(86)90205-5.

Abstract

There are considerable data implicating a pancreatic islet 12-lipoxy-genase in glucose-induced insulin secretion. This enzyme traditionally is conceived as converting unesterified arachidonic acid to "free" hydroperoxyeicosatetraenoic acid and metabolites thereof. However, studies employing the provision of exogenous metabolites of arachidonic acid to islet tissue fail to identify convincingly the mediator of insulin release. It is proposed that the islet lipoxygenase directly peroxidizes unsaturated fatty acids esterified within membrane phospholipids, leading to changes in ion flux and enzyme activity (particularly phospholipase A2) at the membrane level. The release of unesterified metabolites of arachidonate, although reflecting islet lipoxygenase activity, may be an epiphenomenon.

摘要

有大量数据表明胰腺胰岛12-脂氧合酶参与葡萄糖诱导的胰岛素分泌。传统上认为这种酶将未酯化的花生四烯酸转化为“游离”氢过氧化二十碳四烯酸及其代谢产物。然而，向胰岛组织提供花生四烯酸外源性代谢产物的研究未能令人信服地确定胰岛素释放的介质。有人提出，胰岛脂氧合酶直接使膜磷脂中酯化的不饱和脂肪酸过氧化，导致膜水平的离子通量和酶活性（特别是磷脂酶A2）发生变化。花生四烯酸未酯化代谢产物的释放虽然反映了胰岛脂氧合酶的活性，但可能是一种附带现象。