Nutrient regulation of gamma-aminobutyric acid release from islet beta cells

Diabetologia
A SmismansDaniel Pipeleers

Abstract

Glutamate decarboxylase (GAD) of pancreatic beta cells seems to be involved in the development of autoimmune reactivities which occur in insulin-dependent diabetes mellitus. Little is known about the regulation and role of the GAD activity in normal beta cells. In the betaTC6 line, the enzymatic product, gamma-aminobutyric acid (GABA) was reported to be released under glucose stimulation, thus supporting the concept that GABA transmits a suppressive action of glucose-stimulated beta cells on neighbouring alpha cells. In this study GABA was found to be released from normal rat beta cells. Over 24-h culture periods, the released amounts represented a constant fraction (25% per h) of the cellular GABA content. Cellular GABA content and release were dose-dependently increased by the glutamine concentration in the medium; both values decreased following a sustained (24 h) glucose activation (culture at 10 or 20 mmol/l glucose instead of 3 mmol/l). The variations in the medium GABA content did not parallel the changes in insulin release, indicating that both beta-cell secretory products follow different routes of storage and release. We suggest that beta cells can discharge GABA via exocytosis of microvesicles storing GABA as well as...Continue Reading

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