Home FOR AUTHORS General Physiology and Biophysics 2019 General Physiology and Biophysics Vol.38, No.3, p.237–244, 2019

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

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General Physiology and Biophysics Vol.38, No.3, p.237–244, 2019

Title: Transcutaneous carbon dioxide attenuates impaired oxidative capacity in skeletal muscle in hyperglycemia model
Author: T. Matsumoto, M. Tanaka, R. Nakanishi, M. Takuwa, T. Hirabayashi, K. Ono, T. Ikeji, N. Maeshige, Y. Sakai, T. Akisue, H. Kondo, A. Ishihara, H. Fujino

Abstract: Hyperglycemia impairs oxidative capacity in skeletal muscle. Muscle oxidative capacity is regulated by peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α). Transcutaneous carbon dioxide (CO2) enhances PGC-1α expression in skeletal muscle. Therefore, the aim of this study was to clarify the effects of CO2 therapy on muscle oxidative capacity impaired by streptozotocin (STZ)-induced hyperglycemia. Eight-week-old male Wistar rats were randomly divided into 4 groups: control, CO2 treatment, STZ-induced hyperglycemia, and STZ-induced hyperglycemia treated with CO2. STZ-induced hyperglycemia resulted in a decrease of muscle oxidative capacity and decreased PGC-1α and cytochrome c oxidase subunit 4 (COX-4) expression levels; while, application of transcutaneous CO2 attenuated this effect, and enhanced the expression levels of endothelial nitric oxide synthesis (eNOS). These results indicate that transcutaneous CO2 improves impaired muscle oxidative capacity via enhancement of eNOS and PGC-1α-related signaling in the skeletal muscle of rats with hyperglycemia.

Keywords: Carbon dioxide, Muscle oxidative capacity, Hyperglycemia
Published online: 06-Jun-2019
Year: 2019, Volume: 38, Issue: 3 Page From: 237, Page To: 244

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