It is well known that glucocorticoids increase some specific metabolic action of T3 in vitro and in vivo. The retinoid X receptor (RXRs) is an auxiliary protein that heterodimerizes with thyroid hormone receptors (T3R) and enhances its binding to thyroid hormone response elements in target genes. Current evidence suggests that T3R/RXR heterodimer plays a major role in mediating the transcriptional activation of target genes. In this study we aimed at exploring whether the increase in some specific metabolic action of T3 in liver involves the participation of T3R and RXR. We evaluated the effect of Dexamethasone (Dex) administration (250 ug/100g BW every 12 h for 48 h) to adult male Wistar rats on: 1) T3R b protein levels (Western Blot), 2) T3R b mRNA levels (Northern Blot) and 3) RXR protein levels (Western Blot) in liver tissue. The level of nuclear T3R b protein was significantly increased 48 h after Dex administration (arbitary units, mean ± SEM: 177 ±5 (control n = 14) vs 270 ±10 (Dex n = 18), p<0.001). Besides, Dex increased the T3R b mRNA in treated rats vs control rats (arbitary units, mean ± SEM: control = 0,682 ± 0,111 (n = 4), Dex = 1,233 ± 0,203 (n = 3), p<0.05).Under similar conditions, Dex increased the RXR protein levels (arbitrary units, mean ± SEM: control = 0,652 ± 0,004,(n = 5), Dex = 0,804 ± 0,029, (n = 5) , p<0.01). In conclusion, our results indicate that Dex acts increasing the T3R b gene expression and RXR protein levels and these changes could be responsible for the enhanced T3 action on its target genes.
