Abstract

Metabolic changes associated with inflammatory processes and immune response can modify protein and AA requirements. Improved knowledge of these processes will provide opportunities for nutritional intervention to sustain growth and animal defense at the same time. The objective of the study was to identify AA whose metabolism is affected by chronic lung inflammation. Six pairs of littermate piglets were selected at 28 d of age on the basis of their BW. After catheterization of the jugular vein, one littermate received complete Freund's adjuvant (CFA) intravenously, whereas its littermate was injected with a sterile saline solution (CON). Piglets within a litter were pair-fed in order to avoid confounding effects of feed intake and inflammation on plasma AA concentrations. Blood samples were taken after an overnight fast and 2 h after the morning meal for 9 d. Rectal temperature, food consumption, weight gain, plasma haptoglobin, and AA concentrations were measured. The CFA injection decreased food intake, and increased body temperature and plasma haptoglobin concentration. Plasma tryptophan, glutamine, proline, glycine, tyrosine, ornithine, total AA concentrations, and the ratio of tryptophan to large neutral AA were less in CFA than in CON (P < 0.05), independent of time and meal. In contrast, plasma histidine concentration was higher (P < 0.05) in CFA than in CON pigs. Plasma serine, arginine, alanine, asparagine, and total AA concentrations were lower in CFA than in CON pigs only in the fed state (P < 0.05). Among essential AA, only plasma tryptophan concentration was lower (P < 0.01) in CFA than in CON pigs in both fasted and fed state. These results show that chronic lung inflammation affects individual AA differently and suggest that the utilization of some AA increased during chronic lung inflammation in pigs. Activation of tryptophan catabolism enzyme indoleamine 2,3-dioxygenase seems a relevant hypothesis to explain the increased tryptophan utilization, although its incorporation in acute-phase proteins and the existence of other catabolic pathways cannot be excluded.

Full Text
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