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タイトル: | AMPK is indispensable for overload-induced muscle glucose uptake and glycogenesis but dispensable for inducing hypertrophy in mice |
著者: | Kido, Kohei Egawa, Tatsuro https://orcid.org/0000-0001-9363-1589 (unconfirmed) Fujiyoshi, Haruna Suzuki, Hikari Kawanaka, Kentaro Hayashi, Tatsuya https://orcid.org/0000-0001-7600-4735 (unconfirmed) |
著者名の別形: | 木戸, 康平 江川, 達郎 藤吉, 春菜 鈴木, ひかり 林, 達也 |
キーワード: | AMP-activated protein kinase functional overload glucose uptake hypertrophy skeletal muscle |
発行日: | Apr-2021 |
出版者: | Wiley |
誌名: | FASEB journal : official publication of the Federation of American Societies for Experimental Biology |
巻: | 35 |
号: | 4 |
論文番号: | e21459 |
抄録: | Chronic muscle loading (overload) induces skeletal muscles to undergo hypertrophy and to increase glucose uptake. Although AMP-activated protein kinase (AMPK) reportedly serves as a negative regulator of hypertrophy and a positive regulator of glucose uptake, its role in overload-induced skeletal muscle hypertrophy and glucose uptake is unclear. This study aimed to determine whether AMPK regulates overload-induced hypertrophy and glucose uptake in skeletal muscles. To this end, skeletal muscle overload was induced through unilateral synergist ablations in wild-type (WT) and transgenic mice, expressing the dominant-negative mutation of AMPK (AMPK-DN). After 14 days, parameters, including muscle fiber cross-sectional area (CSA), glycogen level, and in vivo [3 H]-2-deoxy-D-glucose uptake, were assessed. No significant difference was observed in body weight or blood glucose level between the WT and AMPK-DN mice. However, the 14-day muscle overload activated the AMPK pathway in WT mice skeletal muscle, whereas this response was impaired in the AMPK-DN mice. Despite a normal CSA gain in each fiber type, the AMPK-DN mice demonstrated a significant impairment of overload-induced muscle glucose uptake and glycogenesis, compared to WT mice. Moreover, 14-day overload-induced changes in GLUT4 and HKII expression levels were reduced in AMPK-DN mice, compared to WT mice. This study demonstrated that AMPK activation is indispensable for overload-induced muscle glucose uptake and glycogenesis; however, it is dispensable for the induction of hypertrophy in AMPK-DN mice. Furthermore, the AMPK/GLUT4 and HKII axes may regulate overload-induced muscle glucose uptake and glycogenesis. |
著作権等: | This is the original submitted manuscript of following article: 'FASEB Journal' Volume35, Issue4, e21459, https://doi.org/10.1096/fj.202002164R. 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/2433/266462 |
DOI(出版社版): | 10.1096/fj.202002164R |
PubMed ID: | 33710687 |
出現コレクション: | 学術雑誌掲載論文等 |
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