Pancreatic Beta Cell Glucose Metabolism and Glibenclamide-lnduced Insulin Release

In order to identify the step(s) of pancreatic intermediate glucose metabolism involved in glibenclamide-stimulated insulin release, 2-deoxy-ghicose and iodoacetamide were used as inhibitors. In situ infusion of the dog pancreas was used as experimental design. While 2-deoxy-glucose did not alter the pattern of glibenclamide-induced insulin release, iodoacetamide at 0.5 or 5 mM concentrations had a clearly inhibitory effect. Sodium pyruvate restored glibenclamide-induced insulin release when impaired by 0.5 mM iodoacetamide but failed to do so when iodoacetamide was used at a 5 mM concentration. The infusion of adenosinetriphosphate (ATP) allowed glibenclamide to cause insulin release in normal amounts, even in the presence of 5 mM iodoacetamide. It is suggested that ATP production resulting from pancreatic intermediate glucose metabolism regulates glibenclamide-induced insulin secretion.