Adegoke, Olasunkanmi A. J.Zerrouk, Miriam2025-11-112025-11-112025-08-182025-11-11https://hdl.handle.net/10315/43326Cancer cachexia is a complex syndrome marked by muscle and fat loss, often resistant to nutritional support. While branched-chain amino acids (BCAAs) stimulate muscle protein synthesis, BCAA-targeted therapies have shown inconsistent results. In this study, a C26 colon cancer mouse model was used to examine how tumor burden alters BCAA metabolism across skeletal muscle, liver, kidney, and adipose tissue. Tumors accumulated BCAAs and showed increased enzymatic activity, whereas peripheral sites displayed widespread BCAA depletion, reduced expression of the amino acid transporter LAT1, and suppression of mechanistic target of rapamycin complex 1 (mTORC1) signaling. Notably, the soleus muscle maintained mTORC1 activity despite reduced BCAA availability, suggesting fiber-type–specific adaptations. These findings indicate that tumors act as metabolic sinks, diverting systemic amino acids away from host tissues. Such reprogramming may underlie the limited success of BCAA-based interventions in cachexia and highlight the need for therapies that address both tumor and host metabolism.Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.KinesiologyHealth sciencesPhysiologyElectronic Thesis or Dissertation2025-11-11Cancer cachexiaBranched-chain amino acidsAmino acid metabolismC26 colon cancer modelSkeletal musclesAmino acid transportersBCKD activitymTORC1 signalingTumor metabolismPeripheral organs