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Glucagon, secreted by the alpha-cells of the pancreatic islets, is the most important glucose-increasing hormone of the body. The precise regulation of glucagon release remains incompletely defined but has been proposed to involve release of inhibitory factors from neighbouring beta-cells (paracrine control). However, the observation that glucose can regulate glucagon secretion under conditions when insulin secretion does not occur argues that the alpha-cell is also equipped with its own intrinsic (exerted within the alpha-cell itself) glucose sensing. Here we consider the possible mechanisms involved with a focus on ATP-regulated K(+)-channels and changes in alpha-cell membrane potential.

Original publication




Journal article


Trends Endocrinol Metab

Publication Date





277 - 284


Animals, Diabetes Mellitus, Glucagon, Glucagon-Secreting Cells, Glucose, Humans, Hypoglycemic Agents, KATP Channels, Membrane Potentials, Models, Biological, Paracrine Communication, Tolbutamide