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The beta-cell response to oral hypoglycemic agents.

作者信息

Cook D L

机构信息

Department of Physiology and Biophysics, School of Medicine, University of Washington, Seattle 98195, USA.

出版信息

Diabetes Res Clin Pract. 1995 Aug;28 Suppl:S81-9. doi: 10.1016/0168-8227(95)01088-u.

DOI:10.1016/0168-8227(95)01088-u
PMID:8529522
Abstract

This review describes the role of sulfonylureas and ATP-sensitive K channels (KATP) in controlling glucose-induced membrane electrical activity in pancreatic beta-cells. The glucose-dependent pathway, the most important both physiologically and pathophysiologically, is contrasted with other pathways for non-nutrient beta-cell modulators. KATP channels, the links between beta-cell metabolism and membrane electrical activity, are regulated in complex ways by nucleotide phosphates and a number of clinically important pharmacological agents. Recent cloning of the islet sulfonylurea receptor and KATP channel should lead to answers to important questions raised by 25 years of beta-cell electrophysiology.

摘要

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