The role of somatostatin and KATP channels in the control of glucagon secretion by glucose

Abstract

Glucagon secreted by α-cells of the islets of Langerhans is the principal hyperglycemic hormone of the body. So far, the mechanisms by which glucose controls glucagon release remain unclear. In this study, we investigate the possible implication of paracrine factors including somatostatin (SST) released by δ-cells, γ-hydroxybutyrate (GHB) released by β-cells and the role of α-cell KATP channels in the control of glucagon secretion by glucose. We show that at low concentrations (0-7 mM), glucose inhibits glucagon secretion independently of SST. The contribution of SST to the glucagonostatic effect of glucose becomes more important at higher concentrations of the sugar (15-30 mM). We also show that the glucagonostatic effect of glucose is independent of GHB as well as α-cell KATP channels. These findings may offer new understanding to clarify the mechanisms responsible for the alteration of glucagon release observed in type 1 and type 2 diabetes(BIFA - Sciences biomédicales et pharmaceutiques) -- UCL, 202