Open AccessArachidonic Acid Metabolism and Insulin Secretion by Isolated Human Pancreatic Islets
Author(s) -
John Turk,
Jonathan H. Hughes,
Richard A. Easom,
Bryan A. Wolf,
David W. Scharp,
Paul E. Lacy,
Michael L. McDaniel
Publication year - 1988
Publication title -
diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.219
H-Index - 330
eISSN - 1939-327X
pISSN - 0012-1797
DOI - 10.2337/diab.37.7.992
Subject(s) - medicine , endocrinology , arachidonic acid , lipoxygenase , cyclooxygenase , pancreatic islets , insulin , islet , metabolism , prostaglandin e2 , chemistry , secretion , prostaglandin e , endogeny , prostaglandin , biology , biochemistry , enzyme
Isolated human pancreatic islets converted [3H8]arachidonate to compounds with the high-performance liquid-chromatographic mobility of cyclooxygenase products, including prostaglandin E2 (PGE2), PGF2 alpha, and the lipoxygenase product 12-HETE. Human islet synthesis of PGE2, PGF2 alpha, and 12-HETE from endogenous arachidonate was demonstrated with stable isotope dilution-gas chromatographic-negative ion-chemical ionization-mass spectrometric analysis. Pharmacologic inhibition of arachidonate metabolism by both lipoxygenase and cyclooxygenase pathways with BW 755C strongly suppressed glucose-induced insulin secretion from perifused human islets, and the selective cyclooxygenase inhibitor indomethacin enhanced insulin secretion. These findings are similar to those reported for islets isolated from rats and suggest that arachidonate metabolites may modulate glucose-induced insulin secretion in humans.
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