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The Walter B Cannon Physiology in Perspective Lecture, 2007 ATP-sensitive K+ channels and disease: from molecule to malady Ashcroft FMAm J Physiol Endocrinol Metab 2007[Oct]; 293 (4): E880-9This 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.|Adenosine Triphosphate/metabolism[MESH]|Animals[MESH]|Channelopathies/*etiology/genetics[MESH]|Diabetes Mellitus/congenital/genetics/therapy[MESH]|Glucose/metabolism[MESH]|Homeostasis/genetics/physiology[MESH]|Humans[MESH]|Models, Biological[MESH]|Models, Molecular[MESH]|Mutation[MESH]|Potassium Channels, Inwardly Rectifying/genetics[MESH]|Potassium Channels/chemistry/genetics/*physiology[MESH] |
