The control of glucagon secretion by glucose and KATP channel modulators
(2014) Proceedings of the Belgian Royal Academies of Medicine — Vol. 3, p. 129-145 (2014)
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- Glucagon secreted by pancreatic α-cells is a hyperglycemic hormone which plays a major role in the correction of hypoglycemia. Its secretion is physiologically controlled by nutrients, hormones and neurotransmitters. The mechanisms by which glucose inhibits its release are poorly known. In particular, it is unclear whether the glucagonostatic effect of glucose results from a direct action on α-cells or an indirect mechanism involving the release of an inhibitory paracrine factor from insulin-secreting β-cells or somatostatin-secreting δ–cells. We briefly review the different hypotheses of the glucagonostatic effect of glucose, and present our own data. In particular, we show that in α-cells, as in β-cells, KATP channels transduce changes in cell metabolism into changes in membrane potential and Ca2+ influx through voltage-dependent Ca2+ channels. A direct closure of α-cell KATP channels stimulates glucagon release and, hence, would not be responsible of the glucagonostatic effect of glucose. By contrast, a direct closure of δ-cell KATP channels stimulates somatostatin release leading to inhibition of glucagon secretion. The net effect of KATP channel blockers on glucagon release result therefore from a balance between a direct stimulatory action on α-cells and an indirect inhibitory action via δ-cells
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Gilon, P., Cheng-Xue, R., Gomez Ruiz, A., Antoine, N., & Chae, H. (2014). The control of glucagon secretion by glucose and KATP channel modulators. Proceedings of the Belgian Royal Academies of Medicine, 3, 129-145. https://hdl.handle.net/2078.5/198188 (Original work published 2014)