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ATP-sensitive K+ (KATP) channels in pancreatic β-cells couple glucose metabolism to insulin secretion. Reduced KATP channel activity produces excessive insulin release and hyperinsulinism whereas increased KATP channel activity leads to lower insulin secretion and diabetes. Paradoxically, mice with genetic deletion of KATP channels, or loss-of-function mutations, are only transiently hypoglycaemic during the neonatal period and often display reduced glucose-stimulated insulin secretion subsequently. Mice with KATP channel gain-of-function mutations are hyperglycaemic and have impaired glucose-stimulated insulin secretion, a phenotype that accurately mimics human diabetes. This review discusses how mice expressing altered KATP channels have provided valuable insight into β-cell function.

Original publication




Journal article


Drug Discov Today Dis Models

Publication Date





e101 - e109