The metabolic response after sepsis is characterized by net protein loss. N
utritional intervention often Is applied to sustain whole body protein mass
under such circumstances. The manner in which protein metabolism of the di
fferent organs is affected under nutrition-supported and postseptic circums
tances remains ambiguous. Therefore, we explored the changes in in vivo org
an and whole body protein turnover after endotoxin-induced sepsis during en
teral nutrition in pigs. The use of isotopes enabled simultaneous measureme
nts of protein synthesis, breakdown and amino acid degradation across the p
ortal-drained viscera (PDV; approximate to intestine), liver and hindquarte
r ( approximate to 50% skeletal muscle). All pigs received a continuous ent
eral 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 per
formed 1 d before and 1 and 4 d after endotoxemia that was induced by a 24-
h endotoxin (3 mug(.)kg bw(-1.)h(-1) lipopolysaccharide, n = 7) infusion. C
ontrols received NaCl (n = 7). At 4 d after endotoxemia, hindquarter protei
n 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 pr
otein synthesis was enhanced 1 d after endotoxemia. Increased amino acid tr
ansamination in hindquarter and PDV led to glutamine and alanine effluxes t
hat serve as substrates for liver and, possibly, the immune system. By prov
iding substrate, enteral nutrition can sustain elevated amino acid demand i
n the postendotoxemic state by hindquarter, PDV and liver for protein synth
esis and transamination processes.