Ionic, Electrical, and Secretory Effects of Inhibitors of Arachidonic-acid Metabolism in Mouse Pancreatic Beta-cells
(1992) Diabetes — Vol. 41, n° 5, p. 620-626 (1992)
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- Mouse islets were used to study the effects of inhibitors of cyclooxygenase and lipoxygenase pathways on insulin release, ionic fluxes, and beta-cell membrane potential. The cyclooxygenase inhibitors, Na-salicylate and Na-acetylsalicylate, potentiated glucose-induced insulin release, despite a decrease in Ca influx evidenced by inhibition of the Ca-dependent electrical activity in beta-cells and Ca-45 efflux from islets perifused with a medium containing Ca. This paradox can probably be explained by a mobilization of intracellular Ca (acceleration of Ca-45 efflux in the absence of Ca) with subsequent activation of K+ channels (acceleration of Rb-86 efflux) and repolarization of the membrane. These effects of salicylate could not be ascribed to a change in intracellular pH because they were not mimicked by 2-Cl-benzoate, which has a similar pK as salicylate but increased insulin release by stimulating Ca influx in beta-cells. Among the other cyclooxygenase inhibitors tested, indomethacin caused a slight potentiation of insulin release accompanied by marginal increases in Ca-45 efflux and electrical activity, whereas flurbiprofen and ibuprofen were ineffective. Among the lipoxygenase inhibitors, compound BW 755c reversibly decreased glucose-induced insulin release by inhibiting Ca influx in beta-cells, but nordihydroguaiaretic acid had no effect. Inhibitors of arachidonic acid metabolism have effects on ionic fluxes and beta-cell membrane potential, which may explain some of the changes in insulin release they produce.
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Drews, G., Garrino, MG., & Henquin, J.-C. (1992). Ionic, Electrical, and Secretory Effects of Inhibitors of Arachidonic-acid Metabolism in Mouse Pancreatic Beta-cells. Diabetes, 41(5), 620-626. https://doi.org/10.2337/diabetes.41.5.620 (Original work published 1992)