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

Abstract

Gastrointestinal (GI) tract leucine metabolism was measured in 6- to 9-mo-old lambs subjected to trickle infection with Trichostrongylus colubriformis larvae and in separate animals that were not infected. Animals prepared with a jejunal catheter and with indwelling catheters into the aorta and the portal- (PDV) and mesenteric- (MDV) drained viscera were infused simultaneously with [1-13C] and [5,5,5-2H3] leucine to determine GI tract sequestration of leucine from arterial and luminal amino acid pools by tracer and tracee arteriovenous concentration differences. Leucine oxidative losses and net fluxes were also determined across the GI tract. Infection had no detectable effect on whole-body leucine flux, but it increased total GI tract leucine sequestration by 24% (P<.05) and GI tract oxidative losses of leucine 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 proportion 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.

Intestinal amino acid absorption in lambs fed fresh Lucerne (Medicago sativa) during an established Trichostrongylus colubriformis infection

“…Possible reasons for the discrepancies between the current study and previous studies with respect to DM flow at the ileum (Gregory et al, 1985), N flow (Poppi et al, 1986;Kimambo et al, 1988) and intestinal absorption (Yu et al, 2000) may be due to the infection procedure used, namely the short-term dose in the current study and the trickle dose methods used by these authors. It is likely that the damage caused by the larvae could affect the ability of the intestine to transport AA.…”

“…This suggests an increase in AA disappearance from the small intestine of the infected lambs, although the apparent absorption from the small intestine and net flux of AA across the MDV were similar between treatments. The net flux of AA across the MDV in the current study (1 to 5 g/day) is similar to the 4 to 6 g/day reported by MacRae et al (1997b) at similar intakes, but the similar net fluxes of AA across the MDV between control and parasitised lambs contrast with the observations for leucine by Yu et al (2000). While mesenteric plasma flows are within the ranges in the literature for sheep at a similar age and DM intake (700 to 1000 ml/min; Janes et al, 1985;MacRae et al, 1997b;Yu et al, 2000;Bermingham et al, 2007b), they are highly variable (CV of 28% to 40% in the control and parasitised lambs, respectively), and this variability may have masked any effects of infection on MDV AA fluxes.…”

“…The net flux of AA across the MDV in the current study (1 to 5 g/day) is similar to the 4 to 6 g/day reported by MacRae et al (1997b) at similar intakes, but the similar net fluxes of AA across the MDV between control and parasitised lambs contrast with the observations for leucine by Yu et al (2000). While mesenteric plasma flows are within the ranges in the literature for sheep at a similar age and DM intake (700 to 1000 ml/min; Janes et al, 1985;MacRae et al, 1997b;Yu et al, 2000;Bermingham et al, 2007b), they are highly variable (CV of 28% to 40% in the control and parasitised lambs, respectively), and this variability may have masked any effects of infection on MDV AA fluxes. High variability (.25%) in blood flow across the MDV has been observed previously (MacRae et al, 1997b;Yu et al, 2000), and might be attributed to either incomplete mixing of the dye in those blood vessels or movement of the catheter due to peristaltic intestinal contractions (MacRae et al, 1997b).…”

“…While changes in leucine absorption and metabolism in the small intestine during parasite infection have been observed previously (Yu et al, 2000), there has been no report on the direct impact of parasitic infection on the intestinal absorption of other AA. Due to the preferential use of AA such as glutamate (Reeds et al, 2000) and the unique AA composition of the gastrointestinal tract (MacRae and Lobley, 1991), there is reason to believe that AA other than leucine may behave differently in the small intestine of parasitised animal.…”

“…This is likely to be the cause of the increased fractional protein synthesis in the small intestine (Symons and Jones, 1975;Bermingham et al, 2006) and leucine oxidation and protein turnover in the gastrointestinal tract (Yu et al, 2000) that have been observed during parasitic infection.…”