Splanchnic metabolism of nutrients and hormones in steers fed alfalfa under conditions of increased absorption of ammonia and L-arginine supply across the portal-drained viscera1,2,3

Abstract

Effects of increased ammonia and/or arginine absorption on net splanchnic (portal-drained viscera [PDV] plus liver) metabolism of nonnitrogenous nutrients and hormones in cattle were examined. Six Hereford x Angus steers (501 +/- 1 kg BW) prepared with vascular catheters for measurements of net flux across the splanchnic bed were fed a 75% alfalfa:25% (as-fed basis) corn and soybean meal diet (0.523 MJ of ME/[kg BW(0.75).d]) every 2 h without (27.0 g of N/kg of DM) and with 20 g of urea/kg of DM (35.7 g of N/kg of DM) in a split-plot design. Net flux measurements were made immediately before and after a 72-h mesenteric vein infusion of L-arginine (15 mmol/h). There were no treatment effects on PDV or hepatic O2 consumption. Dietary urea had no effect on splanchnic metabolism of glucose or L-lactate, but arginine infusion decreased net hepatic removal of L-lactate when urea was fed (P < 0.01). Net PDV appearance of n-butyrate was increased by arginine infusion (P < 0.07), and both dietary urea (P < 0.09) and arginine infusion (P < 0.05) increased net hepatic removal of n-butyrate. Dietary urea also increased total splanchnic acetate output (P < 0.06), tended to increase arterial glucagon concentration (P < 0.11), and decreased arterial ST concentration (P < 0.03). Arginine infusion increased arterial concentration (P < 0.07) and net PDV release (P < 0.10) and tended to increase hepatic removal (P < 0.11) of insulin, as well as arterial concentration (P < 0.01) and total splanchnic output (P < 0.01) of glucagon. Despite changes in splanchnic N metabolism, increased ammonia and arginine absorption had little measurable effect on splanchnic metabolism of glucose and other nonnitrogenous components of splanchnic energy metabolism.

Estimating the energetic cost of feeding excess dietary nitrogen to dairy cows

“…Regulation of urea transport across the rumen wall (Rojen et al, 2011), for example, decouples the extent of N recycling from N intake making the number of biochemical transformations that a N-containing molecule undergoes before excretion impossible to estimate at this time. Maltby et al (2005) found that ureagenesis accounted for <5% of liver O 2 consumption when they measured hepatic O 2 consumption in steers fed high-protein diets. Thus, the additional energy required for metabolizing and excreting N beyond the energy required for ureagenesis is likely the result of several different biochemical and metabolic processes.…”

Degradation of L-arginine and N-carbamoyl glutamate and their effect on rumen fermentationin vitro

“…As a precursor of polyamines and nitric oxide (NO), ARG could improve nitrogen metabolism, angiogenesis and lactogensis (Morris, 2006;Kim and Wu, 2009). L-arginine supplementation increases milk production in cattle and growth hormone in sheep (Chew et al,1984;Davenport et al, 1990aDavenport et al, , 1990b, plasma flow in the portal and hepatic veins in steers (Maltby et al, 2005), and stimulates the production of luteinizing hormone in prepubertal ewes (Recabarren et al, 1996). Recently, injected Arg-HCl has decreased embryonic loss in ewes (Luther et al, 2008), increased lamb birth weight in gestationally nutrient restricted ewes (Lassala et al, 2010), and improved fetal lamb survival to term in prolific ewes (Lassala et al, 2011).…”

Splanchnic net balance of oxygen and metabolites in response to a discontinuous mesenteric vein infusion of ammonium in sheep

“…Thus, ‐stimulated ureagenesis could reduce the energy available for productive purposes. In experiments in vivo where portal flow was increased continuously, liver O 2 consumption linked to metabolism varied, however, from no change (Maltby et al., 2005a,b) to 1.2 mol O 2 /mol converted to urea (Milano et al., 2000), with the interpretation of the data complicated either because of the relatively small increase in liver uptake (Maltby et al., 2005a,b) or the confounding effects of higher amino acid absorption across the PDV (Milano et al., 2000). In addition, appears to interfere with liver glucose metabolism.…”