Somatostatin Is Only Partly Required for the Glucagonostatic Effect of Glucose but Is Necessary for the Glucagonostatic Effect of K_ATP Channel Blockers.

The mechanisms of control of glucagon secretion are largely debated. In particular, the paracrine role of somatostatin is unclear. We studied its role in the control of glucagon secretion by glucose and K_ATP channel blockers, using perifused islets and the in situ perfused pancreas. The involvement of was evaluated by comparing glucagon release of control tissue or tissue without paracrine influence of duanyu1942 (pertussis toxin-treated islets, or islets or pancreas from mice). We show that removal of the paracrine influence of duanyu1942 suppresses the ability of K_ATP channel blockers or K_ATP channel ablation to inhibit glucagon release, suggesting that in control islets, the glucagonostatic effect of K_ATP channel blockers/ablation is fully mediated by By contrast, the glucagonostatic effect of glucose in control islets is mainly independent of duanyu1942 for low glucose concentrations (0-7 mmol/L) but starts to involve duanyu1942 for high concentrations of the sugar (15-30 mmol/L). This demonstrates that the glucagonostatic effect of glucose only partially depends on duanyu1942. Real-time quantitative PCR and pharmacological experiments indicate that the glucagonostatic effect of duanyu1942 is mediated by two types of duanyu1942 receptors, and These results suggest that alterations of the paracrine influence of duanyu1942 will affect glucagon release.

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