Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/19/2009
Publication Date: 3/1/2010
Citation: Freetly, H.C., Ferrell, C.L., Archibeque, S.L. 2010. Net Flux of Amino Acids Across the Portal-drained Viscera and Liver of the Ewe During Abomasal Infusion of Protein and Glucose. Journal of Animal Science. 88(3):1093-1107. Interpretive Summary: Providing adequate protein is important to allow ruminants to produce milk, meat, and fiber at a level to support efficient animal production. However, providing excessive nitrogen to animals potentially contributes to nitrogen contamination of air and water from animal waste. Improved efficiency of nitrogen utilization by the animal improves production efficiency and reduces the negative impact of animal excretions on the environment. Approximately 20% of the protein absorbed by the intestines is used to provide a source of energy to the intestines. When the protein is used for energy, the nitrogen in the protein is excreted. A potential way to reduce the amount of protein used for energy is to provide the intestine an alternative source of energy. Research conducted at the U.S. Meat Animal Center determined that providing elevated levels of glucose as a potential alternative energy source did not improve the rate that amino acids (protein) entered into the blood.
Technical Abstract: Decreasing the fraction of amino acids metabolized by the mucosal cells may increase the fraction of AA being released into the blood. A potential mechanism to reduce AA catabolism by mucosal cells is to provide an alternative source of energy. We hypothesized that increasing glucose flow to the small intestine would increase net appearance of AA across the portal-drained viscera (PDV). Eighteen mature ewes with sampling catheters were placed on study in an extended Latin Square design. Samples were collected over five periods. One-half of the ewes received abomasal glucose infusions (3.84 g/h), and all ewes received each of five protein abomasal infusion levels over five periods (0, 18.1, 36.3, 54.4, and 72.6 AA mmol/h). Net PDV release of isoleucine, leucine, methionine, phenylalanine, glutamate, glutamine, proline, serine, and tyrosine increased linearly (P < 0.05) with increased AA infusion, and net PDV release of histidine, lysine, threonine, valine, alanine, aspartate, and glycine did not differ (P > 0.05) with AA infusion. Net hepatic glucose release decreased with glucose infusion (P = 0.007). With the exception of histidine, lysine, phenylalanine, and valine, net hepatic AA uptake increased linearly with increased molar delivery of AA to the liver (P < 0.005). Glucose infusion increased the hepatic lysine, phenylalanine, and valine uptake with respect to molar delivery rate (P < 0.05). Based on the observations in the current study, we reject our hypothesis that glucose can spare AA metabolism by PDV tissue. Our findings suggest that hepatic gluconeogenesis can be increased in the presence of increased AA delivery to the liver and that hepatic gluconeogenesis can be decreased with increased absorption of dietary glucose. Our findings support the concept that for most AA, hepatic transport of AA can be described by mass action kinetics; however, the rates of hepatic uptake of specific AA are up-regulated directly or indirectly by elevated glucose.