Subclinical infection with the nematode Trichostrongylus colubriformis increases gastrointestinal tract leucine metabolism and reduces availability of leucine for other tissues

Gastrointestinal (GI) tract leucine metabolism was measured in 6- to 9-mo-o ld lambs subjected to trickle infection with Trichostrongylus colubriformis larvae and in separate animals that were not infected. Animals prepared wi th a jejunal catheter and with indwelling catheters into the aorta and the portal- (PDV) and mesenteric- (MDV) drained viscera were infused simultaneo usly with [1-C-13] and [5,5,5-H-2(3)] leucine to determine GI tract sequest ration of leucine from arterial and luminal amino acid pools by tracer and tracee arteriovenous concentration differences. Leucine oxidative losses an d net fluxes were also determined across the GI tract. Infection had no det ect-able effect on whole-body leucine flux, but it increased total GI tract leucine sequestration by 24% (P <.05) and GI tract oxidative losses of leu cine by 22 to 41% (P <.01). Net PDV fluxes of leucine were decreased by 20 to 32% during the infection. The infection did not alter either the proport ion of precursor leucine used by GI tract metabolism that was derived from the arterial leucine pool (.84 to .88) or the proportional sequestration of digesta-derived leucine during "first pass" absorptive metabolism (.12 to .18). These findings help to elucidate the metabolic basis for the reduced growth rates and nitrogen retention observed when animals are subjected to subclinical nematode infection.