2012 Fiscal Year Final Research Report
Effect of AMPK activation on mechanisms responsible for exercise-induced expression of monocarboxylate transporter
| Project/Area Number |
22500616
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Sports science
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| Research Institution | Osaka University of Health and Sport Sciences |
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Principal Investigator |
HAMADA Taku 大阪体育大学, 体育学部, 准教授 (00466294)
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| Co-Investigator(Kenkyū-buntansha) |
HAYASHI Tatsuya 京都大学, 大学院・人間・環境学研究科, 教授 (00314211)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 運動 / MCT / AMPK |
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| Research Abstract |
The purpose of this study was to examine the hypothesis that signaling molecules AMPKwould mediate the acute exercise-induced expression of monocarboxylate transporters MCT1and MCT4 in skeletal muscle. The male SD rats were subjected to a bout of high-intensityintermittent swimming (HIS) or low-intensity prolonged swimming exercise (LIS). AMPKphosphorylation was increased in response to LIS and HIS in exercised muscle. MCT1 andMCT4 mRNA were transiently upregulated by HIS and LIS. MCT1 protein was increased afterLIS, but MCT4 protein was increased after HIS, while no changes in MCT1 protein wereobserved. Direct exposure of epitrochlearis to 0.5mM 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) or 1mM caffeine increased both MCT1 and MCT4 mRNA but notMCT1 and MCT4 protein. When 1mM caffeine-induced pAMPK was inhibited by dantrolene,neither MCT1 nor MCT4 mRNA was increased. The present findings suggest that acute exercisemay upregulate MCT1 and MCT4 mRNA expression thrg-mediated pathway in skeletalmuscle.
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