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Sulfonylureas are widely used to treat non-insulin dependent diabetes mellitus. These drugs exert their hypoglycaemic effects by stimulating insulin secretion from the pancreatic beta-cell. Their primary mechanism of action is to close ATP-sensitive K-channels in the beta-cell plasma membrane, and so initiate a chain of events which results in insulin release. Recent studies have shown that the beta-cell ATP-sensitive K-channel is a complex of two proteins: a pore-forming subunit (Kir6.2) and a drug-binding subunit (SUR1) which functions as the receptor for sulfonylureas. This review summarizes recent advances in our understanding of the molecular mechanism of sulfonylurea action, focusing on the relationship between the sulfonylurea receptor and the K-ATP channel. Earlier studies are also re-examined in the light of new findings.

Original publication

DOI

10.1055/s-2007-979837

Type

Journal article

Journal

Horm Metab Res

Publication Date

09/1996

Volume

28

Pages

456 - 463

Keywords

ATP-Binding Cassette Transporters, Adenosine Triphosphate, Blood Glucose, Cloning, Molecular, Humans, Hypoglycemic Agents, Potassium Channels, Potassium Channels, Inwardly Rectifying, Receptors, Drug, Sulfonylurea Compounds, Sulfonylurea Receptors