Mouse models of β-cell K channel dysfunction

Journal article

ATP-sensitive K (K) channels in pancreatic β-cells couple glucose metabolism to insulin secretion. Reduced K channel activity produces excessive insulin release and hyperinsulinism whereas increased K channel activity leads to lower insulin secretion and diabetes. Paradoxically, mice with genetic deletion of K 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 K 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 K channels have provided valuable insight into β-cell function. © 2013 Elsevier Ltd. All rights reserved.

Authors: Brereton, M; Ashcroft, F

• Journal: Drug Discovery Today: Disease Models
• Publication date: 2013-01-01
• DOI: 10.1016/j.ddmod.2013.02.001
• EISSN: 1740-6757
• ISSN: 1740-6757