The beta-cell response to oral hypoglycemic agents.

This review describes the role of sulfonylureas and ATP-sensitive K channels (KATP) in controlling glucose-induced membrane electrical activity in pancreatic beta-cells. The glucose-dependent pathway, the most important both physiologically and pathophysiologically, is contrasted with other pathways for non-nutrient beta-cell modulators. KATP channels, the links between beta-cell metabolism and membrane electrical activity, are regulated in complex ways by nucleotide phosphates and a number of clinically important pharmacological agents. Recent cloning of the islet sulfonylurea receptor and KATP channel should lead to answers to important questions raised by 25 years of beta-cell electrophysiology.