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Branched‐chain amino acids protect against dexamethasone‐induced soleus muscle atrophy in rats
Author(s) -
Yamamoto Daisuke,
Maki Taiki,
Herningtyas Elizabeth Henny,
Ikeshita Nobuko,
Shibahara Hiromi,
Sugiyama Yuka,
Nakanishi Shiho,
Iida Keiji,
Iguchi Genzo,
Takahashi Yutaka,
Kaji Hidesuke,
Chihara Kazuo,
Okimura Yasuhiko
Publication year - 2010
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.21621
Subject(s) - dexamethasone , endocrinology , medicine , muscle atrophy , soleus muscle , atrophy , autophagy , chemistry , skeletal muscle , biology , biochemistry , apoptosis
We investigated the utility of branched‐chain amino acids (BCAA) in dexamethasone‐induced muscle atrophy. Dexamethasone (600 μg/kg, intraperitoneally) and/or BCAA (600 mg/kg, orally) were administered for 5 days in rats, and the effect of BCAA on dexamethasone‐induced muscle atrophy was evaluated. Dexamethasone decreased total protein concentration of rat soleus muscles. Concomitant administration of BCAA reversed the decrease. Dexamethasone decreased mean cross‐sectional area of soleus muscle fibers, which was reversed by BCAA. Dexamethasone increased atrogin‐1 expression, which has been reported to play a pivotal role in muscle atrophy. The increased expression of atrogin‐1 mRNA was significantly attenuated by BCAA. Furthermore, dexamethasone‐induced conversion from microtubule‐associated protein 1 light chain 3 (LC3)‐I to LC3‐II, which is an indicator of autophagy, was blocked by BCAA. These findings suggest that BCAA decreased protein breakdown to prevent muscle atrophy. BCAA administration appears to be useful for prevention of steroid myopathy. Muscle Nerve, 2010