We have also reported the effectiveness of BCAA in protecting against muscle atrophy in a hindlimb suspension-induced muscle atrophy rat model. mTOR plays an important role in these actions of BCAA. mTOR is involved in the protein synthesis that is stimulated by BCAA and in the protein degradation that is suppressed by BCAA. Several mechanisms by which BCAA stimulates mTOR activity have been proposed, although the precise mechanism remains unclear. The proposed pathway by which mTOR Naloxone hydrochloride action is stimulated is not the same as the pathway utilized byIGF-1 and is not dependent on PI3K.These findings suggest a possible protective action of BCAA against muscle atrophy in the absence of GH/IGF-1. We hypothesized that BCAA would exert a protective effect against Dex-induced muscle atrophy in GH-deficient rats and tested this hypothesis in the present study. However, unexpectedly, we found that Dex and BCAA failed to modulate muscle mass and mTOR signaling in GH deficient rats and that GH reversed the actions of Dex and BCAA. In the present study, we found that Dex failed to modulate muscle mass in SDRs. In the SDRs, Dex did not decrease the CSAs of the muscle fibers but did decrease these CSAs after GH administration. Dex did not elevate Solifenacin succinate atrogin-1 or MuRF1 mRNA levels in the SDR muscles, but Dex did increase the levels of these mRNAs in the muscles of the normal SD rats. However, following GH administration, the increases in atrogin-1 and MuRF1 were observed in the SDRs. These findings are consistent with the responses of the REDD1, FoxO3 and FoxO4 mRNAs. These mRNAs have been reported to be increased by Dex in normal rats. In the present study, Dex did not increase REDD1, FoxO3 or FoxO4 mRNAs in the SDRs but did increase these mRNAs after GH administration. Britto etal. Reported that REDD1 protein expression was increased 5 hours after the Dex administration but not detected 24hours after the administration, indicating the time-dependent expression of REDD1. Because the muscles were removed 18 hours after the last Dex administration in the present study, REDD1 expressions might have been reduced at the sampling of SDR muscles.