Inflammatory burden and @entity535 metabolism in @entity5 XXXX .

@entity1 @entity32 @entity650 @entity5 @entity535 @entity310 @entity3085 @entity448 @entity2057 @entity204
PURPOSE OF REVIEW: Cancer @entity3085 is associated with marked alterations in skeletal muscle protein metabolism that lead to @entity2057 and, in some cases, @entity204 . The inflammatory response elicited by @entity5 is a likely, if not primary, mediator of these alterations. This review focuses on the possible relationship between inflammatory signaling and altered @entity535 metabolism in @entity5 . RECENT FINDINGS: Loss of skeletal muscle in @entity5 @entity1 can potentially be due to @entity448 and early satiety, reduced muscle protein synthesis, and/or increased muscle protein breakdown. @entity32 has been associated with each of these mechanisms. Effects on appetite appear to be mediated by the melanocortin system in the hypothalamus. Studies in animal models of @entity3085 suggest that modulation of orexigenic and anorexigenic pathways in this system may improve nutrient consumption. Inflammatory cytokines such as @entity650 and @entity310 are likely to contribute to the effects of @entity32 on muscle protein metabolism through several pathways. SUMMARY: Limited studies in @entity1 suggest that targeted anti-inflammatory and nutritional interventions may ameliorate the net catabolic effect on skeletal muscle protein metabolism. Future studies of the precise mechanism of muscle protein loss, as well as novel or combination therapies to inhibit @entity32 and promote anabolism, are warranted.
