論文

査読有り 国際誌
2019年5月

Transcutaneous carbon dioxide attenuates impaired oxidative capacity in skeletal muscle in hyperglycemia model.

General physiology and biophysics
  • Tomohiro Matsumoto
  • ,
  • Masayuki Tanaka
  • ,
  • Ryosuke Nakanish
  • ,
  • Mihi Takuwa
  • ,
  • Takumi Hirabayashi
  • ,
  • Kohei Ono
  • ,
  • Takuya Ikeji
  • ,
  • Noriaki Maeshige
  • ,
  • Yoshitada Sakai
  • ,
  • Toshihiro Akisue
  • ,
  • Hiroyo Kondo
  • ,
  • Akihiko Ishihara
  • ,
  • Hidem Fujino

38
3
開始ページ
237
終了ページ
244
記述言語
英語
掲載種別
DOI
10.4149/gpb_2018048

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.

リンク情報
DOI
https://doi.org/10.4149/gpb_2018048
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/31184310

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