期刊
FEBS LETTERS
卷 583, 期 13, 页码 2225-2230出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2009.05.050
关键词
Potassium channel; Kv-channel; Pancreatic beta-cell; Insulin secretion; Glucose metabolism
资金
- Japan Society for the Promotion of Science [20591070, 19045026]
- Salt Science Research Foundation [08C5]
- Japan Diabetes Foundation
- Jichi Medical University
- Grants-in-Aid for Scientific Research [20591070, 19045026] Funding Source: KAKEN
Regulation of delayed rectifier-type K+ channels (Kv-channels) by glucose was studied in rat pancreatic beta-cells. The Kv-channel current was increased in amplitudes by increasing glucose concentration from 2.8 to 16.6 mM, while it was decreased by 2.8 mM glucose in a reversible manner (down-regulation) in both perforated and conventional whole-cell modes. The current was decreased by FCCP, intrapipette 0 mM ATP or AMPPNP. Glyceraldehyde, pyruvic acid, 2-ketoisocaproic acid, and 10 mM MgATP prevented the down-regulation induced by 2.8 mM or less glucose. The residual current after treatment with Kv2.1-specific blocker, guangxitoxin-1E, was unchanged by lowering or increasing glucose concentration. We conclude that glucose metabolism regulates Kv2.1 channels in rats beta-cells via altering MgATP levels. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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