Cited by 21Ion channel regulation and functionPancreatic function and diabetesIon Transport and Channel Regulation

Regulation of voltage‐gated K+ channels by glucose metabolism in pancreatic β‐cells

Yoshida, Masashi, Dezaki, Katsuya, Yamato, Shiho, Aoki, Atsushi, Sugawara, Hitoshi, Toyoshima, Hideo, Ishikawa, San-e, Kawakami, Masanobu +3 more·2009·FEBS Letters

Abstract

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 16.6mM, while it was decreased by 2.8mM glucose in a reversible manner (down-regulation) in both perforated and conventional whole-cell modes. The current was decreased by FCCP, intrapipette 0mM ATP or AMPPNP. Glyceraldehyde, pyruvic acid, 2-ketoisocaproic acid, and 10mM MgATP prevented the down-regulation induced by 2.8mM 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.

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Crossref · 10.1016/j.febslet.2009.05.050

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  • The magnitude of the voltage-gated K+ current increases in response to glucose and other stimulators of β-cell metabolism and is reduced by the mitochondrial inhibitor FCCP or by intracellular dialysis with ATP-free medium or non-hydrolyzable ATP analogues.

    “The magnitude of the voltage-gated K+ current has been reported to increase in response to glucose and other stimulators of β-cell metabolism (including glyceraldehyde and α-ketoisocaproic acid) and is reduced by the mitochondrial inhibitor FCCP or by intracellular dialysis with ATP-free medium or non-hydrolyzable ATP analogues. (753).”

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Authors
Yoshida, M., Dezaki, K., Yamato, S., Aoki, A., Sugawara, H., Toyoshima, H., Ishikawa, S.-E., Kawakami, M., Nakata, M., Yada, T., & Kakei, M.
Affiliations
Jichi Medical University (JP)
Corresponding author
Kakei, Masafumi
Venue
FEBS Letters
Publisher
Wiley
Published
2009-06-03
Volume
583
Issue
13
Pages
2225-2230
ISSN
  • 0014-5793 (ISSN-L)
  • 1873-3468
OpenAlex
W2078510041
Cited by
21
References
1
Citations by year
2024: 1 · 2021: 3 · 2019: 2 · 2017: 2 · 2016: 2 · 2015: 1 · 2014: 2 · 2013: 1 · 2012: 3
FWCI
0.94
Type
journal article
Language
en
Open access
closed
Locations
  • FEBS Letters (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Salt Science Research Foundation
  • Jichi Medical University
  • Japan Diabetes Foundation
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
voltage-gated potassium channels, Kv2.1, glucose metabolism, pancreatic beta cells, MgATP, ATP depletion, FCCP, glyceraldehyde, pyruvate
MeSH terms
Adenosine Triphosphate, Animals, Glucose, Kinetics, Male, Temperature, Down-Regulation, Rats, Wistar, Patch-Clamp Techniques, Potassium Channels, Voltage-Gated, Insulin-Secreting Cells, Rats

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