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Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/8263
Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.
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Rats bearing the Yoshida AH-130 ascites hepatoma showed enhanced fractional rates of protein degradation in gastrocnemius muscle, heart, and liver, while fractional synthesis rates were similar to those in non-tumor bearing rats. This hypercatabolic pattern was associated with marked perturbations of the hormonal homeostasis and presence of tumor necrosis factor in the circulation. The daily administration of a goat anti-murine TNF IgG to tumor-bearing rats decreased protein degradation rates in skeletal muscle, heart, and liver as compared with tumor-bearing rats receiving a nonimmune goat IgG. The anti-TNF treatment was also effective in attenuating early perturbations in insulin and corticosterone homeostasis. Although these results suggest that tumor necrosis factor plays a significant role in mediating the changes in protein turnover and hormone levels elicited by tumor growth, the inability of such treatment to prevent a reduction in body weight implies that other mediators or tumor-related events were also involved.
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COSTELLI, Paola, et al. Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model. Journal of Clinical Investigation. 1993. Vol. 92, num. 6, pags. 2783-2789. ISSN 0021-9738. [consulted: 19 of August of 2026]. Available at: https://hdl.handle.net/2445/8263