Analysis of molecular mechanism on the training effects using prohibited doping drugs
Project/Area Number |
17500421
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Sports science
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Research Institution | Kanazawa University |
Principal Investigator |
KITAURA Takashi Kanazawa University, Health Service Center, Asoociate Professor, 保健管理センター, 助教授 (00143868)
|
Project Period (FY) |
2005 – 2006
|
Project Status |
Completed (Fiscal Year 2006)
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Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2006: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2005: ¥3,000,000 (Direct Cost: ¥3,000,000)
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Keywords | doping / differentiation / Notch Signaling / Delta-like1 / Jagged1 / Satellite cells / clenbuterol / Numb / 薬理学 / 生理学 / 筋芽細胞 / MyoDファミリー / Notchシグナル / Delta-like1 / Myostatin / Numb / IGF-1 |
Research Abstract |
Clenbuterol is one of the beta-2 adrenergic receptor agonists with powerful muscle anabolic effects and is prohibited to use as doping drug for athletes. Recently it is well documented that the muscle hypertrophy is associated with an increase in satellite cell number, a proportionate increase in myonuclear number. And it is established that Notch1 becomes activated in satellite cells as they progress from a state of quiescence to one of active proliferation as myogenic precursor cells. However, we already reported that the Notch 1 mRNA showed no changes in both SOL and EDL. Furthermore, the effect of clenbuterol on the Numb, a plasma membrane-associated cytoplasmic protein, regulating differentiation of satellite cells is still not clear. In this study, we tried to examine the hypertrophic effects of clenbuterol on the Numb regulating system of both fast-and slow-twitch muscles. It is said that clenbuterol increased the MyoD as the myogenic master regulator and might induce the muscle
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hypertrophy and the transformation from slow-to fast-twitch muscle. The muscle wet weights increased in both SOL and EDL muscles with clenbuterol. The myogenin mRNA showed the increase in both muscles. The MyoD mRNA increased drastically in SOL. They may explained the accumulated fast-twitch fibers with fiber type transition from slow-to-fast and may explain the muscle hypertrophy in SOL, but not in EDL. However, the IGF-1, MGF, Myostatin, and Notch1 mRNA showed no changes in both SOL and EDL. The Delta-like1 mRNA showed no changes in SOL (CLEB: 100.7±20.3%, Control: 100.0±9.5 %), but significantly increased in EDL (CLEB: 167.3±28.0%, Control: 100.0±25.0 %; P<0.01). The Numb mRNA also showed no changes in SOL (CLEB: 104.1±19.9%, Control: 100.0±10.3 %), but significantly increased in EDL (CLEB: 131.0±20.0%, Control: 100.0± 21.5 %; P<0.05%). The increased Numb in EDL may explain the muscle hypertrophy according to progressed differentiation of myoblast. These results suggested that the hypertrophic effects of drugs should be explained in either myofibers or satellite cells, respectively. But these markers like Notch and Numb are known as the markers of progressive cancer. Therefore, we have to examine the relationship with Notch-signaling system and carcinogenic process by doping drugs. Less
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Report
(3 results)
Research Products
(13 results)