| Abstract |
Iron deficiency (ID) is a potential contributor to skeletal muscle atrophy through disruption of the balance between protein synthesis and degradation. This muscle loss is associated with sarcopenia and locomotive syndrome, conditions that impair mobility and reduce healthy life expectancy. While branched-chain amino acids (BCAA) are known to attenuate dexamethasone-induced muscle atrophy, its effectiveness against ID-induced atrophy has not been fully elucidated. This study aims to investigate the effects of BCAA on ID-induced muscle atrophy in C2C12 myotubes treated with the iron chelator deferoxamine (DFO). Results showed that DFO significantly reduced myotube diameter and upregulated atrogenes such as Atrogin-1 and MuRF-1, accompanied by increased p-AMPK and p-eEF2, and decreased p-Akt levels. BCAA supplementation partially suppressed Atrogin-1 expression but had no effect on MuRF-1 or myotube diameter. Additionally, p-p70S6K was significantly upregulated in the BCAA + DFO group, while p-eEF2 levels remained elevated, similar to the DFO group. These findings suggest that ID may activate alternative catabolic signaling, such as the NF-kB pathway, thereby counteracting the anabolic effects of BCAA via the Akt signaling pathway. Thus, BCAA has limited efficacy in preventing muscle atrophy under iron-deficient conditions. In conclusion, BCAA may partially promote muscle protein synthesis-related signaling pathways, but is insufficient to prevent muscle atrophy induced by ID.
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