Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.
AUTOR(ES)
Costelli, P
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=288478Documentos Relacionados
- Tumor necrosis factor-alpha inhibits albumin gene expression in a murine model of cachexia.
- Cachexia and tumour necrosis factor-alpha in cytomegalovirus infection.
- Tumor necrosis factor-alpha stimulates hepatic lipogenesis in the rat in vivo.
- Tumor necrosis factor-alpha inhibits expression of pulmonary surfactant protein.
- Tumor necrosis factor-alpha modifies adhesion properties of rat islet B cells.