GPBAR1 and cancer: Altogether, these results lead us to exclude a contribution of the TGR5 pathway to the altered myogenic program in C26 mice and to speculate that the selective reduction in TGR5 activation capacity by UDCA in C26 mice may contribute to the exacerbation of the muscle atrophy found in C26 mice only, and vice versa, that TGR5 agonists may hold anti-atrophy therapeutic potential in cancer cachexia.