Influence of glucagon, gastric inhibitory polypeptide, pancreatic polypeptide and somatostatin on beta-adrenergically induced insulin secretion in the mouse.

The effect of four polypeptides, glucagon, Gastric Inhibitory Polypeptide (GIP), Pancreatic Polypeptide (PP) and somatostatin on beta-adrenoceptor stimulated insulin secretion in vivo in the mouse was investigated. The beta-adrenoceptor stimulation was induced by isoprenaline (IPNA). It was found that at dose levels without influence on basal insulin secretion the polypeptides produced the following pattern of interaction with IPNA. Insulin secretion induced by IPNA was increased by glucagon and inhibited by somatostatin. GIP and PP did not change IPNA-induced insulin release. It is concluded from this and earlier published studies that glucagon, but not always GIP, serves as a positive modulator of basal and stimulated insulin secretion, and that somatostatin is a general inhibitor of insulin release. beta-Adrenoceptor-induced insulin secretion however, seems to be less sensitive to somatostatin than insulin release induced by glucose.