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Skeletal muscle hypertrophic effect of clenbuterol is additive to the hypertrophic effect of myostatin suppression
Author(s) -
Kim Kyung Ho,
Kim Yong Soo
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.600.26
Subject(s) - skeletal muscle , endocrinology , medicine , myostatin , muscle hypertrophy , clenbuterol , plantaris muscle , genotype , myocyte , chemistry , biology , soleus muscle , gene , biochemistry
It is well established that myostatin (MSTN) suppression or clenbuterol (CL) administration enhances skeletal muscle mass, but the interaction of MSTN suppression and CL administration on skeletal muscle mass has not been examined. To examine the interaction of MSTN suppression and CL administration on skeletal muscle mass, 35 days old female wild type and heterozygous MSTN‐pro transgenic mice that exhibits 20‐30 % enhanced muscle mass by overexpression of MSTN prodomain were administrated 0 and 20 ppm CL in drinking water for 2 wks. Four different muscle samples from hind legs were collected at 1 wk and 2 wk after CL administration. Regardless of genotype, CL significantly increased the body and muscle mass at 1 wk or 2 wk after CL administration. No significant genotype and CL interactions on body and muscle mass were observed. DNA concentration of plantaris muscle was significantly decreased by CL administration for 1 wk or 2 wk regardless of genotype. RNA concentration of plantaris muscle was significantly increased by CL administration for 1 wk in both genotypes, but no significant change in RNA concentration was observed at 2 wk of CL administration in both genotypes. The RNA/DNA ratio in plantaris muscle was significantly elevated by CL administration for 1 wk or 2 wk in both genotypes. In summary, the result of this study demonstrates that skeletal muscle hypertrophic effect of CL is additive to the hypertrophic effect of MSTN suppression, suggest that the mechanism of action of CL leading to skeletal muscle hypertrophy might be different from that of MSTN.