However, in contrast to SDR muscles in which REDD1mRNA was not increased by Dex, REDD1 mRNA level was markedly induced by Dex in GH-treated SDR muscles. This result indicates that Dex response was restored after LY900009 GH-treatment. There are some discrepancies in REDD2 and myostatin mRNA expressions between previous reports and our results. In the present study, we found that Dex stimulated REDD2 expression. Little is known about the effect of Dex on REDD2 mRNA levels. To the best of our knowledge, effect of Dex on REDD2 mRNA expression in muscles was reported in only one article and Dex had no effect onREDD2mRNA levels in there port. The reason that causes the difference is unknown. It is reported that glucocorticoids increase myostatin mRNA in rat muscles and cultured muscle cells. However, Jesinkey et al. reported that Dex treatment for 7days did not stimulate myostatin mRNA levels in muscles, which is consistent with our result. In the present study, 5 and 6SDRs per one group were used in the Experiment, respectively. The small number of SDRs due to limited availability of SDRs might explain the difference in myostatin mRNA. Some mRNA levels were not significantly influenced by Dex and BCAA, showing just a tendency. These responses also might be explained by the limited number of SDRs. It is difficult to exclude the possibility of the type II error that underestimates significant results. We found that GR mRNA level was higher in the SDR muscles than in the GH-administered SDR muscles or in the normal SD rat muscles. This result suggests that the defect of Dex��s action in SDR muscles is not due to the low expression of GR. Furthermore, Dex administration resulted in decreased body weight in SDRir respective of BCAA or GH administration, indicating bioactivity of Dex was preserved in SDRs. Dex might disturb the pathways that are activated by GH in the muscles, and the Mepivacaine hydrochloride actions of Dex on the muscles might have been unobservable in the absence of GH. A previous up-regulation of CSA by GH might be required for the suppressive effect of Dex, and previous down-regulations ofatrogin-1, MuRF1, REDD1, FoxO3 and FoxO4 mRNA levels by GH might be required for the increase in these mRNA levels that is mediated by Dex.