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タイトル: | Methylglyoxal reduces molecular responsiveness to 4 weeks of endurance exercise in mouse plantaris muscle |
著者: | Egawa, Tatsuro https://orcid.org/0000-0001-9363-1589 (unconfirmed) Ogawa, Takeshi Yokokawa, Takumi https://orcid.org/0000-0002-3813-4958 (unconfirmed) Kido, Kohei Goto, Katsumasa Hayashi, Tatsuya https://orcid.org/0000-0001-7600-4735 (unconfirmed) |
著者名の別形: | 江川, 達郎 小川, 岳史 横川, 拓海 林, 達也 |
キーワード: | exercise resistance glycation insulin signaling mitochondria nonresponder |
発行日: | Feb-2022 |
出版者: | American Physiological Society |
誌名: | Journal of Applied Physiology |
巻: | 132 |
号: | 2 |
開始ページ: | 477 |
終了ページ: | 488 |
抄録: | Endurance exercise triggers skeletal muscle adaptations, including enhanced insulin signaling, glucose metabolism, and mitochondrial biogenesis. However, exercise-induced skeletal muscle adaptations may not occur in some cases, a condition known as exercise-resistance. Methylglyoxal (MG) is a highly reactive dicarbonyl metabolite and has detrimental effects on the body such as causing diabetic complications, mitochondrial dysfunction, and inflammation. This study aimed to clarify the effect of methylglyoxal on skeletal muscle molecular adaptations following endurance exercise. Mice were randomly divided into 4 groups (n = 12 per group): sedentary control group, voluntary exercise group, MG-treated group, and MG-treated with voluntary exercise group. Mice in the voluntary exercise group were housed in a cage with a running wheel, while mice in the MG-treated groups received drinking water containing 1% MG. Four weeks of voluntary exercise induced several molecular adaptations in the plantaris muscle, including increased expression of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α), mitochondria complex proteins, toll-like receptor 4 (TLR4), 72-kDa heat shock protein (HSP72), hexokinase II, and glyoxalase 1; this also enhanced insulin-stimulated Akt Ser<sup>473</sup> phosphorylation and citrate synthase activity. However, these adaptations were suppressed with MG treatment. In the soleus muscle, the exercise-induced increases in the expression of TLR4, HSP72, and advanced glycation end products receptor 1 were inhibited with MG treatment. These findings suggest that MG is a factor that inhibits endurance exercise-induced molecular responses including mitochondrial adaptations, insulin signaling activation, and the upregulation of several proteins related to mitochondrial biogenesis, glucose handling, and glycation in primarily fast-twitch skeletal muscle. |
著作権等: | This is the accepted version of the article and not used for commercial purposes The full-text file will be made open to the public on 4 February 2023 in accordance with publisher's 'Terms and Conditions for Self-Archiving'. This is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。 |
URI: | http://hdl.handle.net/2433/278908 |
DOI(出版社版): | 10.1152/japplphysiol.00539.2021 |
PubMed ID: | 35023763 |
出現コレクション: | 学術雑誌掲載論文等 |
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