Arachidonic acid metabolism and insulin secretion by isolated human pancreatic islets

J. Turk; J. H. Hughes; R. A. Easom; B. A. Wolf; D. W. Scharp; P. E. Lacy; M. L. McDaniel

doi:10.2337/diab.37.7.992

Arachidonic acid metabolism and insulin secretion by isolated human pancreatic islets

J. Turk, J. H. Hughes, R. A. Easom, B. A. Wolf, D. W. Scharp, P. E. Lacy, M. L. McDaniel

Division of Endocrinology, Metabolism & Lipid Research

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Isolated human pancreatic islets converted [³H₈]arachidonate to compounds with the high-performance liquid-chromatographic mobility of cyclooxygenase products, including prostaglandin E₂ (PGE₂), PGF(2α), and the lipoxygenase product 12-HETE. Human islet synthesis of PGE₂, PGF(2α), 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.

Original language	English
Pages (from-to)	992-996
Number of pages	5
Journal	Diabetes
Volume	37
Issue number	7
DOIs	https://doi.org/10.2337/diab.37.7.992
State	Published - 1988

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title = "Arachidonic acid metabolism and insulin secretion by isolated human pancreatic islets",

abstract = "Isolated human pancreatic islets converted [3H8]arachidonate to compounds with the high-performance liquid-chromatographic mobility of cyclooxygenase products, including prostaglandin E2 (PGE2), PGF(2α), and the lipoxygenase product 12-HETE. Human islet synthesis of PGE2, PGF(2α), 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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T1 - Arachidonic acid metabolism and insulin secretion by isolated human pancreatic islets

AU - Turk, J.

AU - Hughes, J. H.

AU - Easom, R. A.

AU - Wolf, B. A.

AU - Scharp, D. W.

AU - Lacy, P. E.

AU - McDaniel, M. L.

PY - 1988

Y1 - 1988

N2 - Isolated human pancreatic islets converted [3H8]arachidonate to compounds with the high-performance liquid-chromatographic mobility of cyclooxygenase products, including prostaglandin E2 (PGE2), PGF(2α), and the lipoxygenase product 12-HETE. Human islet synthesis of PGE2, PGF(2α), 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.

AB - Isolated human pancreatic islets converted [3H8]arachidonate to compounds with the high-performance liquid-chromatographic mobility of cyclooxygenase products, including prostaglandin E2 (PGE2), PGF(2α), and the lipoxygenase product 12-HETE. Human islet synthesis of PGE2, PGF(2α), 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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JO - Diabetes

JF - Diabetes

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Arachidonic acid metabolism and insulin secretion by isolated human pancreatic islets

Abstract

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