Gastrin releasing peptide augments glucose mediated 45Ca2+ uptake, electrical activity, and insulin secretion of mouse pancreatic islets.

Gastrin releasing peptide (GRP) has recently been shown to increase glucose-induced insulin secretion in vivo. Being present in pancreatic tissue, the 27-amino acid peptide could play a role in the control of the glucose-induced insulin secretion of islets of Langerhans. In the presence of a stimulatory glucose concentration, GRP augmented insulin secretion of isolated islets in batch incubations. The peptide did not affect 56Rb+ efflux in the presence of 3 or 5.6 mM glucose but reduced the increase of 86Rb+ efflux evoked by the calcium ionophore A23187. 45Ca2+ uptake and intracellular recorded electrical activity induced by glucose were amplified by GRP. It is suggested that GRP plays a role in the regulation of glucose-induced insulin secretion by increasing the uptake of Ca2+ directly or by inhibition of the Ca(2+)-dependent K+ channel activity and reduced repolarization of the cell.