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ISSN 0188-9796 (Print)

2003, Number 3

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Rev Endocrinol Nutr 2003; 11 (3)

Protein turnover in sepsis

Casas RML, Zúñiga RA, Pasquetti CA, Meléndez MG

Language: Spanish
References: 27
Page: 136-141
PDF size: 127.23 Kb.


ABSTRACT

As a result of injury sepsis carries a number of metabolic alterations, mainly increased glucose turnover and gluconeogenesis. Beside sustrate deficiency, muscle catabolism during sepsis is a consequence of both, increased proteolysis and inhibition of protein synthesis, due to hormonal mediation (Insulin, Insulin-like Growth Factor, glucocorticoids) and citokine action (tumor necrosis factor, interleukine-1). All this causes a loss of body protein greater than 0.5 g/kg/d. Current therapy is aimed to lower muscle protein catabolism and to promote increases in lean body mass. Insulin, insulin-like Growth Factor, proteasome inhibitors, glutamine and tumor necrosis factor blockers have been used with these purposes.


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