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Muscle wasting and protein metabolism¹

Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111

² Correspondence: 711 Washington St. (phone: 617-556-3081; fax: 617-556-3083; E-mail: ccastaneda{at}hnrc.tufts.edu).

Abstract

Accelerated muscle proteolysis is the primary cause of muscle wasting in many catabolic diseases such as diabetes mellitus, renal and liver failure, HIV infection and AIDS, and cancer. In individuals with catabolic diseases, as is the case with fasting states (anorexia and starvation), protein breakdown increases while protein synthesis declines, resulting in negative muscle protein balance. The pathway responsible for accelerated proteolysis in catabolic conditions is the ubiquitin-proteosome-dependent system. Muscle proteolysis increases under conditions of acidosis, up-regulation of branched-chain ketoacid dehydrogenase, the presence of catabolic hormones (glucocorticoids, thyrotoxic states), insulin resistance, and multiple cytokines (interleukin-1 and -6 and tumor necrosis factor). In contrast, factors that suppress muscle proteolysis and wasting, leading to a state of adaptation, include dietary protein deficiency with adequate energy intake, use of anabolic agents, and resistance exercise training. The understanding of the biochemical adaptations that reduce protein degradation and improve nitrogen balance are important for the development of effective therapies to combat muscle wasting and improve protein homeostasis with catabolic illnesses.

¹ This work was funded in part by the USDA, ARS, under agreement contract 58-1950-9-001. Any opinions, findings, conclusion, or recommendations expressed in this publication are those of the author(s) and do not necessarily reflect the view of the USDA.

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