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The endocrine part of the pancreas plays a central role in blood-glucose regulation. It is well established that an elevation of glucose concentration reduces secretion of the hyperglycaemia-associated hormone glucagon from pancreatic alpha 2 cells. The mechanisms involved, however, remain unknown. Electrophysiological studies have demonstrated that alpha 2 cells generate Ca2+-dependent action potentials. The frequency of these action potentials, which increases under conditions that stimulate glucagon release, is not affected by glucose or insulin. The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) is present in the endocrine part of the pancreas at concentrations comparable to those encountered in the central nervous system, and co-localizes with insulin in pancreatic beta cells. We now describe a mechanism whereby GABA, co-secreted with insulin from beta cells, may mediate part of the inhibitory action of glucose on glucagon secretion by activating GABAA-receptor Cl- channels in alpha 2 cells. These observations provide a model for feedback regulation of glucagon release, which may be of significance for the understanding of the hypersecretion of glucagon frequently associated with diabetes.

Original publication

DOI

10.1038/341233a0

Type

Journal article

Journal

Nature

Publication Date

21/09/1989

Volume

341

Pages

233 - 236

Keywords

Animals, Bicuculline, Chloride Channels, Chlorides, Electric Conductivity, Glucagon, Glucose, Guinea Pigs, In Vitro Techniques, Islets of Langerhans, Membrane Potentials, Membrane Proteins, Receptors, GABA-A, Secretory Rate, gamma-Aminobutyric Acid