Although glucose and protein metabolism have been investigated extensively in experimental models of hypodynamic sepsis, relatively little information is available regarding the compensated stage of sepsis. We investigated interorgan amino acid and glucose metabolism in a porcine model of compensated hyperdynamic sepsis. Fasting catheterized pigs received endotoxin (Escherichia coli lipopolysaccharide; 3µg·h-1·kg-1; intravenous) or saline (controls) and volume resuscitation over 24h to reproduce hyperdynamic sepsis. Primed-constant infusions of p-aminohippurate and 3H-labelled isotopes were used to measure glucose, amino acid and protein metabolism across the portal-drained viscera, liver and hindquarters (to represent muscle) at 0 and 24h of endotoxaemia. Whole-body protein and glucose flux were increased during hyperdynamic compensated sepsis. In endotoxaemic pigs, visceral protein was conserved, and hindquarter protein breakdown exceeded the increase in liver protein synthesis, resulting in net whole-body protein loss. Endotoxaemia increased hindquarter and visceral glycolysis and branched-chain amino acid transamination. The rate of efflux of glutamine and alanine from the hindquarters was higher than anticipated from protein breakdown, indicating de novo synthesis of these amino acids during endotoxaemia. In addition to the hindquarters, the portal-drained viscera provided substantial gluconeogenic amino acids and lactate to the liver. Although increased liver glutamate release constitutes an important nitrogen-sparing mechanism and carbon skeletons are effectively being cycled in glucose, net body protein is lost through increased ureagenesis during the hyperdynamic stage of sepsis. Specific amino acid requirements may develop in compensated hyperdynamic sepsis that is characterized by maintained organ perfusion and increased substrate utilization at the expense of body protein.
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Research Article|
January 10 2003
Aspects of organ protein, amino acid and glucose metabolism in a porcine model of hypermetabolic sepsis
Maaike J. BRUINS;
1Department of Surgery, Maastricht University, Maastricht, The Netherlands
Correspondence: Dr Maaike J. Bruins, Unilever Health Institute, Unilever Research, P.O. Box 114, NL-3130 AC Vlaardingen, The Netherlands (e-mail maaike.bruins@unilever.com).
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Nicolaas E.P. DEUTZ;
Nicolaas E.P. DEUTZ
1Department of Surgery, Maastricht University, Maastricht, The Netherlands
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Peter B. SOETERS
Peter B. SOETERS
1Department of Surgery, Maastricht University, Maastricht, The Netherlands
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Publisher: Portland Press Ltd
Received:
October 03 2002
Accepted:
November 01 2002
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 2003
2003
Clin Sci (Lond) (2003) 104 (2): 127–141.
Article history
Received:
October 03 2002
Accepted:
November 01 2002
Citation
Maaike J. BRUINS, Nicolaas E.P. DEUTZ, Peter B. SOETERS; Aspects of organ protein, amino acid and glucose metabolism in a porcine model of hypermetabolic sepsis. Clin Sci (Lond) 1 February 2003; 104 (2): 127–141. doi: https://doi.org/10.1042/cs1040127
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