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dc.contributor.author | Kido, Kohei | en |
dc.contributor.author | Egawa, Tatsuro | en |
dc.contributor.author | Fujiyoshi, Haruna | en |
dc.contributor.author | Suzuki, Hikari | en |
dc.contributor.author | Kawanaka, Kentaro | en |
dc.contributor.author | Hayashi, Tatsuya | en |
dc.contributor.alternative | 木戸, 康平 | ja |
dc.contributor.alternative | 江川, 達郎 | ja |
dc.contributor.alternative | 藤吉, 春菜 | ja |
dc.contributor.alternative | 鈴木, ひかり | ja |
dc.contributor.alternative | 林, 達也 | ja |
dc.date.accessioned | 2021-12-06T06:24:15Z | - |
dc.date.available | 2021-12-06T06:24:15Z | - |
dc.date.issued | 2021-04 | - |
dc.identifier.uri | http://hdl.handle.net/2433/266462 | - |
dc.description.abstract | 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. | en |
dc.language.iso | eng | - |
dc.publisher | Wiley | en |
dc.rights | This is the original submitted manuscript of following article: 'FASEB Journal' Volume35, Issue4, e21459, https://doi.org/10.1096/fj.202002164R. | en |
dc.rights | 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。 | en |
dc.subject | AMP-activated protein kinase | en |
dc.subject | functional overload | en |
dc.subject | glucose uptake | en |
dc.subject | hypertrophy | en |
dc.subject | skeletal muscle | en |
dc.title | AMPK is indispensable for overload-induced muscle glucose uptake and glycogenesis but dispensable for inducing hypertrophy in mice | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | FASEB journal : official publication of the Federation of American Societies for Experimental Biology | en |
dc.identifier.volume | 35 | - |
dc.identifier.issue | 4 | - |
dc.relation.doi | 10.1096/fj.202002164R | - |
dc.textversion | author | - |
dc.identifier.artnum | e21459 | - |
dc.identifier.pmid | 33710687 | - |
dcterms.accessRights | open access | - |
datacite.awardNumber | 18J01392 | - |
datacite.awardNumber | 19K20007 | - |
datacite.awardNumber | 18H03148 | - |
datacite.awardNumber | 19K22806 | - |
datacite.awardNumber | 19K11520 | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18J01392/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19K20007/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18H03148/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19K22806/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19K11520/ | - |
dc.identifier.pissn | 0892-6638 | - |
dc.identifier.eissn | 1530-6860 | - |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.awardTitle | 虚血プレコンディショニングによる新規糖代謝改善法の開発 --運動の併用効果に着目して | ja |
jpcoar.awardTitle | 単回レジスタンス運動でインスリン感受性を改善するために --分子制御からのアプローチ | ja |
jpcoar.awardTitle | 糖化ストレスによる運動トレーニング効果の抑制作用の検証 --糖化研究基盤確立に向けて | ja |
jpcoar.awardTitle | カルボニルストレス解毒システムをターゲットとした骨格筋老化抑制の検証 | ja |
jpcoar.awardTitle | 筋収縮によって即時的に活性化される骨格筋糖輸送を増強・減弱する因子とその分子機構 | ja |
出現コレクション: | 学術雑誌掲載論文等 |
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