The skeletal muscle atrophy consists in muscle mass loss and decreased force generation, produced by molecular mechanisms such as oxidative stress and imbalance in synthesis/degradation proteins processes, that generates a reduction in the myofibrillar proteins content. Mitochondrial dysfunction is another mechanism involved in the muscle atrophy, because the mitochondria are mainly linked to the bioenergetic state in muscle, and also in the calcium homeostasis, apoptosis, autophagy and oxidative stress. The skeletal muscle atrophy can be development by several chronic diseases, such as liver disease (CLD), characterized by high plasma levels of bile acids, among them, cholic acid (CA) and deoxycholic acid (DCA). TGR5 had been defined like the only receptor of bile acids expressed in the skeletal muscle, and it had been described as a metabolic regulator in different cell types. Until now, it had not been evaluated the effect of DCA and CA, neither the TGR5 participation in atrophy or in the mitochondrial dysfunction in the skeletal muscle induced by CLD. Based in these antecedents, we proposed this hypothesis: “Cholic acid and Deoxycholic acid, through TGR5 receptor, induce skeletal muscle atrophy and mitochondrial dysfunction in the skeletal muscle”. Three specific objectives were performed by evaluating the effect of DCA and CA in muscle atrophy (objective 1) and mitochondrial dysfunction (objective 2) in skeletal muscle cells. To correlate with a in vivo model, we used a murine model of CLD induced by hepatotoxin in the diet, that present high levels of plasma bile acids (objective 3), using WT y TGR5-/- mice to evaluate the receptor participation. The results shown that DCA and CA produced skeletal muscle atrophy and mitochondrial dysfunction in vitro. The model in vivo shown that mice with CLD shown decreased muscle function and also mitochondrial dysfunction. The effects in both models, in vivo and in vitro were dependent on TGR5 expression. In conclusion, DCA and CA bile acids through TGR5 induce muscle atrophy and mitochondrial dysfunction in skeletal muscle cells, and presumably it can be responsible of the atrophic effects generated in a murine model of CLD that present high levels of bile acids.Gran parte de esta investigación ya fue publicada pero aún queda pendiente la parte mitocondrial.