2013 Fiscal Year Annual Research Report
骨格筋の可塑性に及ぼすβ２‐アドレナリン受容体発現レベルの応答とその機能的役割
| Project/Area Number |
24650409
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| Research Institution | Waseda University |
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Principal Investigator |
今泉 和彦 早稲田大学, 人間科学学術院, 教授 (60145068)
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| Co-Investigator(Kenkyū-buntansha) |
立屋敷 かおる 上越教育大学, その他部局等, その他 (20119324)
白土 健 早稲田大学, 人間科学学術院, 助手 (60559384)
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| Keywords | クレンブテロール / β2‐作動薬 / 骨格筋萎縮 / アドレナリン受容体 / 細胞内情報伝達 / 骨格筋肥大 / 骨格筋の可塑性 / 骨格筋の組織化学 |
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| Research Abstract |
In 2013, we reported that p38 mitogen-activated protein kinase(MAPK) and Akt pathways play a functional role in the adaptation to β2-agonist, clenbuterol(CLE) treatment and exercise, particularly in slow-twitch muscle. Although CLE induces muscle hypertrophy by stimulating protein synthesis, the precise mechanism by which CLE increases muscle power and muscle mass is unknown. Further, CLE selectively causes muscle hypertrophy in fast-twitch muscles, but it is not clear whether its repressive effects on atrophy differ according to skeletal muscle fiber types.
In 2014, therefore, we studied histochemically whether daily administration of CLE(1mg/kg BW/day) prevents casted-immobilization(IMM)-induced atrophy of skeletal muscle fibers. Adult male Sprague-Dawley rats were divided into control, CLE, IMM, and IMM+CLE groups, and were maintained for 9 days. The extensor digitorum longus(EDL) and soleus muscles were isolated and analyzed histochemically after ATPase staining. EDL and soleus muscle weights in the IMM group were lower than those in the control group. Analysis of cross-sectional areas revealed that EDL muscle atrophy was limited to type II fibers; soleus muscle atrophy involved type I and type II fibers. In the IMM+CLE group, IMM-induced muscle atrophy was attenuated in the EDL, but not in the soleus muscle. Moreover, the attenuating effect of CLE was observed in type II fibers. These results suggest that CLE attenuated IMM-induced atrophy of type II fibers in the fast-twitch EDL muscle but not in the slow-twitch soleus muscle.
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