Chronic or acute inflammation may participate in the etiology of cancer cachexia. To investigate the interaction between tumor and a secondary inflammatory stimulus on muscle wasting, rats with and without a tumor (Yoshida ascites hepatoma) received a low dose of endotoxin (LPS 400 µg/kg, s.c.) or saline. Nitrogen balance was measured 24 hours before and after LPS/saline. Epitrochlearis muscle was used to measure in vitro protein metabolism and gastrocnemius muscle was used for quantification of the mRNA for components of the ubiquitin proteolytic pathway. The Yoshida hepatoma reduced muscle mass (p=0.002), increased muscle protein degradation (p=0.042) and elevated mRNA expression of components of the ubiquitin proteolytic pathway (p<0.01) including ubiquitin, ubiquitin conjugating enzyme E214k, and ubiquitin ligases MuRF-1 and atrogin-1. Although the selected low dose of LPS had no impact on protein metabolism in control rats, LPS in rats bearing Yoshida hepatoma caused weight loss (p=0.0007), lowered nitrogen balance (p= <0.0001) and increased muscle protein degradation (p=0.0336). In conclusion, the presence of a tumor can potentiate whole body and muscle-specific catabolic losses of protein, in response to a stimulus that is not catabolic in healthy animals. This effect might be dependent on the inflammatory nature of the tumor.