Glucose-inhibition of glucagon secretion involves activation of GABAA-receptor chloride channels

Patrik Rorsman, Per Olof Berggren, Krister Bokvist, Hans Ericson, Hanns Möhler, Claes Göran Östenson, Paul A. Smith

Research output: Contribution to journalArticlepeer-review

350 Scopus citations


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 α2 cells. The mechanisms involved, however, remain unknown. Electrophysiological studies have demonstrated that α2 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 γ-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 β cells. We now describe a mechnism whereby GABA, co-secreted with insulin from β-cells, may mediate part of the inhibitory action of glucose on glucagon secretion by activating GABA(A)-receptor Cl- channels in α2 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 languageEnglish (US)
Pages (from-to)233-236
Number of pages4
Issue number6239
StatePublished - 1989

ASJC Scopus subject areas

  • General


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