We conducted 2 experiments to determine lysine bioavailability from 2 lipid-coated lysine products. In an in vitro experiment we mixed each lipid-coated lysine product with either alfalfa- or corn-silage at different amounts of acidity. Scanning electron micrographs indicated that surface structure of each lipid-coated lysine particle was eroded after mixing with silage. Additionally, visual evaluation of scanning electron micrographs suggested that peripheral surface abrasion of lipid-coated lysine may be greater when lipid-coated lysine was mixed with alfalfa silage in comparison to corn silage. In a corresponding experiment, in vivo measures of lysine bioavailability to sheep from 2 lipid-coated lysine products and lysine-HCl were determined after mixing in corn silage. Plasma lysine concentrations increased linearly (P < 0.01) in response to abomasal lysine infusion indicating that our model was sensitive to increases in metabolizable lysine flow. Bioavailability of each lipid-coated lysine source and dietary lysine-HCl were calculated to be 23, 15, and 18%, respectively. Even though each dietary source of lysine increased plasma lysine, rates of increases in plasma lysine from one lipid-coated lysine source (linear; P = 0.20) and lysine-HCl (linear; P = 0.11) were not different from plasma lysine levels supported by diet alone. However, the rate of plasma lysine increase in response to lysine from the other lipid-coated lysine source was greater (P = 0.04) than plasma lysine from feed alone. Nonetheless, the rate of plasma lysine increase in response to lipid-coated lysine did not differ (P ≥ 0.70) from the rate of plasma lysine increase from lysine-HCl. Clearly, methods of manufacture, together with physical and chemical characteristics of diet, can impact amounts of metabolizable lysine provided from lipid-coated lysine products. Direct measures of lysine bioavailability from lipid-coated lysine products after mixing with diets should be based on measurements with the products treated similarly to the method of feeding.

We conducted 2 experiments to determine lysine loss from 2 lipid-coated lysine products after mixing with silage. In our first experiment, we mixed 2 lipid-coated lysine products, crystalline lysine or crystalline lysine and amounts of lipid identical to amounts included in lipid-coated lysine products, with alfalfa or corn silage that had 2 different amounts of acidity. Lysine appeared to disassociate from lipid-coated lysine products in a nonlinear manner after mixing with either alfalfa or corn silage at different amounts of acidity. Additionally, silage source and acidity affected amounts of lysine released from lipid-coated lysine products after mixing. In a corresponding experiment, in vitro estimates of lysine available to ruminal microbiota after mixing with alfalfa or corn silage at different amounts of acidity were measured by ammonia release. In vitro measures were conducted with or without monensin to allow estimates of effects of monensin on amounts of lysine released from the 2 lipid-coated lysine products. It is unclear whether in vitro estimates of lysine fermentation from lipid-coated lysine are truly reflective of ruminal degradation of lysine from lipid-coated lysine because amounts of time needed to measure differences between different lysine sources were greater than typical estimates of mean ruminal particulate retention time. Nonetheless, monensin apparently reduced ammonia release from lysine, but ammonia release from lipid-coated lysine did not differ from crystalline lysine. Clearly, methods of manufacture together with physical and chemical characteristics of diet can affect amounts of lysine provided from lipid-coated lysine products to ruminants.

No abstract

To determine the effects of leucine supplementation on body weight (BW), tissue mass, nutrient digestibility, the concentration of serum amino acids (AAs) and metabolites, and protein abundance of elongation initiation factor 4E (eIF4E) in skeletal muscle, 23 Holstein bull calves (43. 3 ± 1.16 kg; 11.3 ± 0.57 days of age) fed milk replacer at 2.5% of body weight (BW; dry matter basis) were used in a randomized complete block design. Leucine was supplemented at 0, 0.4, 0.6, or 0.8 g Leu/kg BW per day for 28 d. Data were analyzed using the MIXED procedure of SAS. Leucine supplementation did not affect calf BW (P = 0.73), and digestibility of nitrogen (P = 0.21), organic matter (P = 0.28), and dry matter (P = 0.28). Masses proportional to BW of the pancreas (P = 0.04), omasum (P < 0.01), and spleen (P = 0.01) were quadratically affected by treatment where tissue mass decreased at 0.4 g Leu/kg BW and increased at 0.6 and 0.8 g Leu/kg BW. Semitendinosus mass proportional to BW tended (P = 0.07) to be quadratically affected, as tissue mass increased at 0.4 g Leu/kg BW, and decreased at 0.6 and 0.8 g Leu/kg BW. Serum Leu concentration increased linearly (P = 0.002; day × time × treatment) across days and after feedings with increased supplemental Leu. Increasing supplemental Leu linearly decreased serum Ala (P < 0.01), Arg (P = 0.04), Ile (P = 0.02), Met (P < 0.01), and Pro (P = 0.05) concentrations, and quadratically affected serum Glu (P = 0.04) and Lys (P = 0.03) concentrations where serum Glu and Lys concentrations were decreased at 0.4 g Leu/kg BW and increased at 0.6 and 0.8 g Leu/kg BW. There was no effect of treatment on protein abundance of eIF4E in semitendinosus or longissimus dorsi. These data indicate that supplemental Leu did not influence ADG and nitrogen retention in calves fed milk replacer. However, changes in serum AA concentrations and tissue masses proportional to BW suggest that supplementation of Leu at lower levels could increase the use of AA for non-visceral tissue growth.

Nutrient requirements of grazing ruminants change throughout the production year. Also, pasture quality and quantity change throughout the year and are influenced by environment. Therefore, there commonly are times of the year where nutrient requirements are not met from the forage alone. We have long known the importance of nutrition during key development including the conception, fetal, neonatal, and weaning period. Altering nutrition during these periods can have lasting effects on health and productivity. Much of the research in ruminants examining nutritional effects on development has focused on large changes in diet, such as energy or protein restriction, rather than specific nutrients such as amino acids. Amino acids play an important role to meet requirements for lean growth but also have other physiological functions regulating metabolism and health that have important effects on development. Amino acid deficiencies during the fetal and neonatal period(s) can result in small-for-gestational age births or stunting, respectively. Diets that are deficient in protein or amino acids are also often deficient in dietary energy and other nutrients. Supplying specific amino acids (and other nutrients/energy) for absorption, signaling, and use by the animal could be an approach to help overcome negative developmental outcomes. Specific amino acids are thought to function by regulating protein synthesis, immune function, 1-C metabolism, intestinal development and health, blood flow, cellular proliferation, and behavior, to name a few. Some of the amino acids with potential for influencing developmental outcomes include leucine, arginine, glutamine, lysine, methionine, threonine, and tryptophan. Because of the varied functional roles of specific amino acids, there is great potential to develop targeted supplementation programs using amino acids to improve developmental outcomes.