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Nitric Oxide (Nitrogen Monoxide, No) Stimulates Insulin Secretion by Inducing Calcium Release from Mitochondria

https://doi.org/10.1006/bbrc.1995.2815Get rights and content

Abstract

Nitric oxide (nitrogen monoxide, NO) acts as messenger molecule in a variety of cells and may also be involved in the insulin secretory pathway of islet β-cells. We report here that NO at a low micromolar concentration stimulates epinephrine-sensitive insulin secretion from cells of the β-cell line, INS-1. Insulin secretion is paralleled by a reversible decrease of the mitochondrial membrane potential and by an increase of the cytosolic calcium. Chelation of intracellular, but not of extracellular calcium prevents the NO-induced insulin secretion. These data indicate that NO can stimulate insulin secretion by deenergizing mitochondria and thereby triggering mitochondrial calcium release.

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    Citation Excerpt :

    Richter found that NO bound to cytochrome oxidase, blocked respiration, and thereby caused mitochondrial deenergization and Ca2+ release [29]. Laffranchi found that NO can stimulate insulin secretion by deenergizing mitochondria and thereby triggering mitochondrial Ca2+ release [30]. Therefore, inhibition of respiration could lead to PTP opening, which in turn could cause the release of Ca2+ from mitochondria.

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