Endotoxemia affects organ protein metabolism differently during prolonged feeding in pigs

M.J. Bruins, P.B. Soeters, N.E.P. Deutz*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


The metabolic response after sepsis is characterized by net protein loss. Nutritional intervention often is applied to sustain whole body protein mass under such circumstances. The manner in which protein metabolism of the different organs is affected under nutrition-supported and postseptic circumstances remains ambiguous. Therefore, we explored the changes in in vivo organ and whole body protein turnover after endotoxin-induced sepsis during enteral nutrition in pigs. The use of isotopes enabled simultaneous measurements of protein synthesis, breakdown and amino acid degradation across the portal-drained viscera (PDV; approximately intestine), liver and hindquarter ( approximately 50% skeletal muscle). All pigs received a continuous enteral infusion of a liquid meal equivalent to 0.3 g protein. kg bw(-1). h(-1) 3 d before and 4 d after a 24-h endotoxemia period. Measurements were performed 1 d before and 1 and 4 d after endotoxemia that was induced by a 24-h endotoxin (3 microg. kg bw(-1). h(-1) lipopolysaccharide, n = 7) infusion. Controls received NaCl (n = 7). At 4 d after endotoxemia, hindquarter protein turnover was increased, resulting in net synthesis. The amino acid output by the PDV was increased 1 and 4 d after endotoxemia. In the liver, net protein synthesis was enhanced 1 d after endotoxemia. Increased amino acid transamination in hindquarter and PDV led to glutamine and alanine effluxes that serve as substrates for liver and, possibly, the immune system. By providing substrate, enteral nutrition can sustain elevated amino acid demand in the postendotoxemic state by hindquarter, PDV and liver for protein synthesis and transamination processes.
Original languageEnglish
Pages (from-to)3003-3013
Number of pages11
JournalJournal of Nutrition
Issue number12
Publication statusPublished - 1 Jan 2000


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