Open AccessREGULATION OF SKELETAL MUSCLE PROTEIN TURNOVER DURING SEPSIS
Author(s) -
Robert N. Cooney,
Scot R. Kimball,
Thomas C. Vary
Publication year - 1997
Publication title -
shock
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.095
H-Index - 117
eISSN - 1540-0514
pISSN - 1073-2322
DOI - 10.1097/00024382-199701000-00001
Subject(s) - sepsis , protein turnover , anabolism , skeletal muscle , catabolism , protein catabolism , wasting , protein degradation , endocrinology , medicine , protein metabolism , tumor necrosis factor alpha , proteolysis , biology , inflammation , hormone , metabolism , protein biosynthesis , biochemistry , enzyme , amino acid
Skeletal muscle protein wasting is a prominent feature of the metabolic response to sepsis. Persistent protein wasting leads to muscle dysfunction and prolongs recovery from the septic insult. Unfortunately, conventional nutritional support alone does not prevent the sepsis-induced weight loss and catabolism of muscle. Hence, mechanisms other than substrate deficiency appear to be involved in the derangements in protein metabolism during sepsis. The catabolism of muscle during sepsis results from a stimulation of proteolysis and an inhibition of protein synthesis. This review summarizes the mechanisms responsible for alterations in protein synthesis and degradation in muscle during sepsis at the biochemical level. The ability of hormones (insulin, insulin-like growth factor I, glucocorticoids) or cytokines (tumor necrosis factor, interleukin-1) to act as mediators of protein catabolism is also examined. Finally, we discuss the potential role of anticytokine therapies in preventing derangements in protein metabolism during sepsis. A picture is emerging which suggests that cytokines may influence skeletal muscle protein metabolism during sepsis both indirectly through inhibition of the regulatory actions of anabolic hormones on protein turnover, and directly through modulation of the protein synthesis and degradation enzymatic machinery.