Mouse models of β-cell K channel dysfunction
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 de...
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| Format: | Journal article |
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2013
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| Summary: | 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. |
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