更清晰的恶病质图景：利用C26荷瘤小鼠的身体成分成像

Cancer cachexia remains a major unmet need in oncology, characterized by progressive loss of skeletal muscle and adipose tissue that negatively impacts treatment tolerance and survival. Anamorelin (AML), a ghrelin receptor agonist, is currently the only approved therapeutic for cancer cachexia; however, its clinical benefits remain modest, highlighting the need for improved preclinical models and more informative physiological endpoints. Here, we established and characterized a C26 colorectal carcinoma cachexia model using both traditional metrics and non-invasive body composition imaging performed on a Bruker MiniSpec. This platform enabled longitudinal quantification of lean and fat mass changes with high sensitivity, providing a refined assessment of cachexia progression and therapeutic response.In vitro and in vivo studies confirmed the robust cachexia-inducing phenotype of the C26 model. Consistent with published literature, AML treatment increased food intake in tumor-bearing mice but did not reduce circulating pro-inflammatory cytokines. Combination therapy, evaluated based on the mechanistic rationale that AML-mediated appetite stimulation may complement the anti-inflammatory activity of CYA, demonstrated enhanced preservation of body mass and adipose tissue compared with either monotherapy. Our findings support the utility of integrating body composition imaging with standard physiological and biochemical measures to generate a comprehensive efficacy profile. These results highlight the value of this refined platform for evaluating emerging cachexia therapeutics and suggest that multi-modal combinations such as CYA+AML may provide superior benefit over current single-agent approaches.