期刊
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
卷 293, 期 4, 页码 E880-E889出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00348.2007
关键词
Kir6.2; SUR1; neonatal diabetes; hyperinsulinism
资金
- Wellcome Trust Funding Source: Medline
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.
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