Interleukin 1-induced prostaglandin E2 accumulation by isolated pancreatic islets

J. H. Hughes, R. A. Easom, B. A. Wolf, J. Turk, M. L. McDaniel

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51 Scopus citations

Abstract

Recombinant human interleukin 1α (IL-1) has been found to induce prostaglandin E2 (PGE2) accumulation by isolated rat islets of Langerhans at concentrations similar to those at which the cytokine inhibits glucose-induced insulin secretion and islet glucose oxidation. Maximal stimulation of PGE2 accumulation (5 times control value) occurred at 200 pM IL-1, and half-maximal stimulation occurred at 25 pM IL-1. Significant augmentation of PGE2 accumulation by IL-1 required 10-18 h of exposure to the cytokine. Islets that had been pretreated with IL-1 for 18 h showed elevated rates of PGE2 production at basal (3-mM) and stimulatory (16.5-mM) glucose concentrations and converted exogenous arachidonic acid to PGE2 at twice the maximal rate of control islets. Exogenous PGE2 did not mimic the inhibitory effects of IL-1 on glucose-induced insulin secretion or glucose oxidation. To rule out the possibility that endogenous PGE2 is involved in the inhibitory effects of IL-1, the effect of a cyclooxygenase inhibitor on IL-1-treated islets was examined. Pharmacological blockade of PGE2 biosynthesis by 10 μM indomethacin did not influence the inhibitory effects of IL-1 on glucose-induced insulin secretion or glucose oxidation. Thus, exogenous PGE2 does not mimic the effects of IL-1 on islets, and inhibition of endogenous PGE2 biosynthesis does not suppress the effects of IL-1 on islets. These results suggest that PGE2 is not a principal mediator of the inhibitory effects of IL-1 on glucose-induced insulin secretion or glucose oxidation.

Original languageEnglish
Pages (from-to)1251-1257
Number of pages7
JournalDiabetes
Volume38
Issue number10
DOIs
StatePublished - Jan 1 1989

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