Hirano T, Fukuyama S, Nagano S, Takahashi T
Endocrinol Jpn. 1984 Oct;31(5):549-55. doi: 10.1507/endocrj1954.31.549.
The effect of exogenous arachidonic acid on insulin secretion was investigated in a perifusion system using isolated hamster pancreatic islets. Exogenous arachidonic acid (10, 20, 50, 100 micrograms/ml) markedly stimulated glucose-induced insulin release. The enhancement of insulin release by arachidonic acid was completely inhibited by the cyclooxygenase inhibitor, sodium salicylate (0.5 mg/ml). In contrast to this, lipoxygenase inhibitor, nordihydroguaiaretic acid (10(-4) M), enhanced arachidonic acid-induced insulin secretion. Arachidonic acid hydroperoxide inhibited glucose-induced insulin release. Exogenous PG E2 (10(-5) M) potently elevated immunoreactive insulin (IRI) values throughout perifusion. These results suggest that the enhancement of insulin release by exogenous arachidonic acid is derived from newly synthetized prostaglandins and on the other hand, activation of the lipoxygenase pathway inhibits arachidonic acid-induced insulin secretion by decreasing the synthesis of prostaglandins.
利用分离的仓鼠胰岛在灌流系统中研究了外源性花生四烯酸对胰岛素分泌的影响。外源性花生四烯酸（10、20、50、100微克/毫升）显著刺激葡萄糖诱导的胰岛素释放。花生四烯酸对胰岛素释放的增强作用被环氧化酶抑制剂水杨酸钠（0.5毫克/毫升）完全抑制。与此相反，脂氧合酶抑制剂去甲二氢愈创木酸（10⁻⁴ M）增强了花生四烯酸诱导的胰岛素分泌。花生四烯酸氢过氧化物抑制葡萄糖诱导的胰岛素释放。外源性前列腺素E2（10⁻⁵ M）在整个灌流过程中有效提高免疫反应性胰岛素（IRI）值。这些结果表明，外源性花生四烯酸对胰岛素释放的增强作用源自新合成的前列腺素，另一方面，脂氧合酶途径的激活通过减少前列腺素的合成来抑制花生四烯酸诱导的胰岛素分泌。
