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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(+) (K(ATP)) channel in glucose homeostasis and, in particular, on its role in insulin secretion from pancreatic beta-cells. The beta-cell K(ATP) 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 K(ATP) channel structure and function, and consider how mutations in the K(ATP) channel genes lead to neonatal diabetes or congenital hyperinsulinism.

Original publication

DOI

10.1152/ajpendo.00348.2007

Type

Journal article

Journal

Am J Physiol Endocrinol Metab

Publication Date

10/2007

Volume

293

Pages

E880 - E889

Keywords

Adenosine Triphosphate, Animals, Channelopathies, Diabetes Mellitus, Glucose, Homeostasis, Humans, Models, Biological, Models, Molecular, Mutation, Potassium Channels, Potassium Channels, Inwardly Rectifying