We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Roles of ATP-Sensitive K[sup+] Channels as Metabolic Sensors.
- Authors
Minami, Kohtaro; Miki, Takashi; Kadowaki, Takashi; Seino, Susumu
- Abstract
ATP-sensitive K[sup+] channels (K[subATP] channels) are present in various tissues, including pancreatic β-cells, heart, skeletal muscles, vascular smooth muscles, and brain. K[subATP] channels are hetero-octameric proteins composed of inwardly rectifying K[sup+] channel (Kir6.x) and sulfonylurea receptor (SUR) subunits. Different combinations of Kir6.x and SUR subunits comprise K[subATP] channels with distinct electrophysiological and pharmacological properties. Recent studies of genetically engineered mice have provided insight into the physiological and pathophysiological roles of Kir6.x-containing [subATP] channels. Analysis of Kir6.2 null mice has shown that Kir6.2/SUR1 channels in pancreatic β-cells and the hypothalamus are essential in glucose-induced insulin secretion and hypoglycemia-induced glucagon secretion, respectively, and that Kir6.2/SUR2 channels are involved in glucose uptake in skeletal muscles. Kir6.2-containing K[subATP] channels in brain also are involved in protection from hypoxia-induced generalized seizure. In cardiovascular tissues, Kir6.1-containing K[subATP] channels are involved in regulation of vascular tonus. In addition, the Kir6.1 null mouse is a model of Prinzmetal angina in humans. Our studies of Kir6.2 null and Kir6.1 null mice reveal that K[subATP] channels are critical metabolic sensors in acute metabolic changes, including hyperglycemia, hypoglycemia, ischemia, and hypoxia. Diabetes 53 (Suppl. 3): S176-S180, 2004
- Subjects
ADENOSINE triphosphate; POTASSIUM channels; TISSUES; PANCREATIC beta cells; VASCULAR smooth muscle; ELECTROPHYSIOLOGY; PATHOLOGICAL physiology; HYPOTHALAMUS; INSULIN; PANCREATIC secretions; HYPOXEMIA; HYPOGLYCEMIA; HYPERGLYCEMIA; ISCHEMIA
- Publication
Diabetes, 2004, Vol 53, pS176
- ISSN
0012-1797
- Publication type
Article
- DOI
10.2337/diabetes.53.suppl_3.S176