Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.
Skip to main content

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.

Original publication




Journal article


Drug Discovery Today: Disease Models

Publication Date