Beta-carotene increases muscle mass and hypertrophy in the soleus muscle in mice
2015
Kitakaze, T. (Osaka Prefecture University, Sakai, Osaka (Japan). Graduate School of Life and Environmental Sciences, Division of Applied Life Sciences) | Harada, N. | Imagita, H. | Yamaji, R.
Supplements and naturally occurring nutraceuticals effective for maintenance or enhancement of skeletal muscle mass are expected to contribute to prevention of decreased mobility and increased risk of developing metabolic diseases. However, information about available food components remains widely unavailable. In the present study, we investigated the effects of dietary beta-carotene on the quantity and quality of skeletal muscle under physiological conditions. Male ddY mice (8 wk old) were orally administered beta-carotene (0.5 mg once daily) for 14 d. Dietary beta-carotene had no influence on body weight, but increased the soleus muscle/body weight ratio. The cross-sectional area (CSA) in muscle fibers of the soleus muscle was increased, indicating that administration of beta-carotene induces muscle hypertrophy. In the soleus muscle of the beta-carotene-administered mice, twitch force tended to be increased (p=0.06) and tetanic force was significantly increased, whereas specific force (force per CSA) remained unchanged. Dietary beta-carotene increased the mRNA level of insulin-like growth factor 1 (Igf-1) as its splicing variant Igf-1ea, but had no influence on the liver Igf-1 mRNA level or serum IGF-1 level. Beta-Carotene promoted protein synthesis in the soleus muscle and reduced levels of ubiquitin conjugates, but had no influence on the mRNA levels of two atrogenes, Atrogin-1 and Murf1. On the other hand, beta-carotene had no influence on the processing of the autophagy marker protein light chain 3. These results indicate that in mice, administration of beta-carotene increases mass and induces functional hypertrophy in the soleus muscle, perhaps by promoting IGF-1-mediated protein synthesis and by reducing ubiquitin-mediated protein degradation.
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