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Am J Physiol Endocrinol Metab 293: E880-E889, 2007. First published July 24, 2007; doi:10.1152/ajpendo.00348.2007
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THE WALTER B. CANNON PHYSIOLOGY IN PERSPECTIVE LECTURE, 2007

ATP-sensitive K+ channels and disease: from molecule to malady

Frances M. Ashcroft

Henry Wellcome Centre for Gene Function, University of Oxford, Oxford, United Kingdom

This essay is based on a lecture given to the American Physiological Society in honor of Walter B. Cannon, an advocate of homeostasis. It focuses on the role of the ATP-sensitive potassium K+ (KATP) channel in glucose homeostasis and, in particular, on its role in insulin secretion from pancreatic beta-cells. The beta-cell KATP channel comprises pore-forming Kir6.2 and regulatory SUR1 subunits, and mutations in either type of subunit can result in too little or too much insulin release. Here, I review the latest information on the relationship between KATP channel structure and function, and consider how mutations in the KATP channel genes lead to neonatal diabetes or congenital hyperinsulinism.

Kir6.2; SUR1; neonatal diabetes; hyperinsulinism


Address for reprint requests and other correspondence: F. M. Ashcroft, Henry Wellcome Centre for Gene Function, Dept. of Physiology, Anatomy and Genetics, Univ. of Oxford, Parks Road, Oxford OX1 3PT, UK (e-mail: frances.ashcroft{at}dpag.ox.ac.uk)




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