Abstract
Gastric inhibitory polypeptide (GIP), an incretin candidate, is suggested to amplify the glucose-induced insulin secretion. To evaluate its mode of action we examined whether GIP affects 86Rb + efflux, 45Ca 2+ uptake or efflux, and intracellularly recorded electrical activity of mouse pancreatic islets. GIP (5 nM) neither inhibited 86Rb + efflux at 3 mM glucose nor modulated 86Rb + efflux that was inhibited by 5.6 mM glucose or stimulated by the calcium ionophore A23187. 45Ca 2+ uptake was increased by GIP in the presence of 16.7 mM which was not observed at 3 or 11 mM glucose. GIP elevated 45Ca 2+ efflux from islets, but did not modify 45Ca 2+ efflux when a virtually Ca 2+ free medium was used. Electrical activity of beta cells induced by 16.7 mM glucose was significantly increased by 5 nM GIP. It is concluded that the amplification of insulin release by GIP is based on the effect of GIP on Ca 2+ uptake.
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