Abstract
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.
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