title: The Walter B. Cannon Physiology in Perspective Lecture, 2007. ATP-sensitive K+ channels and disease: from molecule to malady.
abstract: 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.
authors.affiliation: Henry Wellcome Centre for Gene Function, Dept. of Physiology, Anatomy and Genetics, Univ. of Oxford, Parks Road, Oxford OX1 3PT, UK. frances.ashcroft@dpag.ox.ac.uk
authors.forename: Frances M
authors.initials: FM
authors.lastname: Ashcroft
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D053447:Channelopathies / Q000209:etiology* / Q000235:genetics; D003920:Diabetes Mellitus / Q000151:congenital / Q000235:genetics / Q000628:therapy; D005947:Glucose / Q000378:metabolism; D006706:Homeostasis / Q000235:genetics / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D008958:Models, Molecular; D009154:Mutation; D015221:Potassium Channels / Q000737:chemistry / Q000235:genetics / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying / Q000235:genetics; D000099161:Kcnj11 Channel
chemical_list: D000255:Adenosine Triphosphate; D005947:Glucose; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D000099161:Kcnj11 Channel