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Regulation of voltage‐gated K + channels by glucose metabolism in pancreatic β‐cells
Author(s) -
Yoshida Masashi,
Dezaki Katsuya,
Yamato Shiho,
Aoki Atsushi,
Sugawara Hitoshi,
Toyoshima Hideo,
Ishikawa San-e,
Kawakami Masanobu,
Nakata Masanori,
Yada Toshihiko,
Kakei Masafumi
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.05.050
Subject(s) - chemistry , medicine , endocrinology , metabolism , biophysics , carbohydrate metabolism , pyruvic acid , biochemistry , biology
Regulation of delayed rectifier‐type K + channels (Kv‐channels) by glucose was studied in rat pancreatic β‐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 β‐cells via altering MgATP levels.