Whole-body and splanchnic amino acid metabolism in sheep during an acute endotoxin challenge.

Supplemented protein or specific amino acids (AA) are proposed to help animals combat infection and inflammation. The current study investigates whole-body and splanchnic tissue metabolism in response to a lipopolysaccharide (LPS) challenge with or without a supplement of six AA (cysteine, glutamine, methionine, proline, serine and threonine). Eight sheep were surgically prepared with vascular catheters across the gut and liver. On two occasions, four sheep were infused through the jugular vein for 20 h with either saline or LPS from Escherichia coli (2 ng/kg body weight per min) in a random order, plus saline infused into the mesenteric vein; the other four sheep were treated with saline or LPS plus saline or six AA infused via the jugular vein into the mesenteric vein. Whole-body AA irreversible loss rate (ILR) and tissue protein metabolism were monitored by infusion of [ring-2H2]phenylalanine. LPS increased (P<0·001) ILR (+17 %), total plasma protein synthesis (+14 %) and lymphocyte protein synthesis (+386 %) but decreased albumin synthesis (-53 %, P=0·001), with no effect of AA infusion. Absorption of dietary AA was not reduced by LPS, except for glutamine. LPS increased the hepatic removal of leucine, lysine, glutamine and proline. Absolute hepatic extraction of supplemented AA increased, but, except for glutamine, this was less than the amount infused. This increased net appearance across the splanchnic bed restored arterial concentrations of five AA to, or above, values for the saline-infused period. Infusion of key AA does not appear to alter the acute period of endotoxaemic response, but it may have benefits for the chronic or recovery phases.

Responses in whole-body amino acid kinetics to an acute, sub-clinical endotoxin challenge in lambs.

Some effects of parasitism, endotoxaemia or sepsis can be mitigated by provision of extra protein. Supplemented protein may encompass a metabolic requirement for specific amino acids (AA). The current study investigates a method to identify and quantify the amounts of AA required during inflammation induced by an endotoxin challenge. One of each pair of six twin sheep was infused in the jugular vein for 20 h with either saline (control) or lipopolysaccharide (LPS, 2 ng/kg body weight per min) from Escherichia coli. Between 12 and 20 h a mixture of stable isotope-labelled AA was infused to measure irreversible loss rates. From 16 to 20 h all sheep were supplemented with a mixture of unlabelled AA infused intravenously. Blood samples were taken before the start of infusions, and then continuously over intervals between 14 and 20 h. At 20 h the sheep were euthanised, and liver and kidney samples were taken for measurement of serine-threonine dehydratase (SDH) activity. LPS infusion decreased plasma concentrations of most AA (P<0·05; P<0·10 for leucine and tryptophan), except for phenylalanine (which increased P=0·022) and tyrosine. On the basis of the incremental response to the supplemental AA, arginine, aspartate, cysteine, glutamate, lysine (tendency only), glycine, methionine, proline, serine and threonine were important in the metabolic response to the endotoxaemia. The AA infusion between 16 and 20 h restored the plasma concentrations in the LPS-treated sheep for the majority of AA, except for glutamine, isoleucine, methionine, serine and valine. LPS treatment increased (P<0·02) SDH activity in both liver and kidney. The approach allows quantification of key AA required during challenge situations.

Effect of intensification of pastoral farming on greenhouse gas emissions in New Zealand.

In 2007, greenhouse gas (GHG) emissions in New Zealand were 16% higher than in 1990. Agriculture accounts for 48% of GHG emissions in New Zealand, and 10-12% of emissions in most other 'developed' countries. Methane (CH4) accounts for 35% of GHG emissions in New Zealand, mostly from ruminal fermentation. Nitrous oxide (N2O) accounts for 17% of GHG emissions in New Zealand, mostly from urinary N, exacerbated by excessive application of nitrogenous fertiliser. GHG are often expressed as carbon dioxide equivalents (CO2-e), and 1 kg CH4 has a similar global-warming potential as 21 kg CO2, whilst 1 kg N2O has the same warming potential as 310 kg CO2. Methane is derived from H2 produced during ruminal fermentation, and losses account for 6-7% of gross energy in feeds. This is about 9-10% of metabolisable energy intake. Methane production tends to be lower when legumes, rather than grasses, are fed, and emissions are greater (per kg dry matter intake; DMI) when mature grasses and silages are fed. There are small differences between individual animals in their CH4 production (g/kg DMI) but there are few profitable options available for reducing CH4 production in ruminants. Emissions of N2O can be reduced by more strategic application of nitrogenous fertiliser, avoidance of waterlogged areas, and use of dicyandiamide in some cooler regions. GHG mitigation should be based on life-cycle analyses to ensure a reduction in one GHG does not increase another. Current and future strategies are unlikely to reduce GHG emissions by >20%. Food production is central to human survival, and should not be compromised to mitigate GHG emissions. Efforts should be directed toward increasing animal efficiency and reducing GHG emissions/unit edible food.

Effect of feed intake on amino acid transfers across the ovine hindquarters.

Responses in variables of amino acid (AA) metabolism across peripheral tissues to feed intake were studied in six sheep (mean live weight 32 kg) prepared with arterio-venous catheters across the hindquarters. Four intakes (0.5, 1.0, 1.5 and 2.5 x maintenance energy) were offered over 2-week periods to each sheep in a Latin square design with two animals replicated. Animals were infused intravenously with a mixture of U-13C-labelled AA for 10 h and integrated blood samples withdrawn from the aorta and vena cava hourly between 5 and 9 h of infusion. Biopsy samples were also taken from skin and m. vastus lateralis. Data from both essential (histidine, isoleucine, leucine, lysine, phenylalanine, threonine) and nonessential (glycine, proline, serine, tyrosine) AA were modelled to give rates of inward and outward transport, protein synthesis and degradation, plus the fraction of total vascular inflow that exchanged with the hindquarter tissues. Rates of inward transport varied more than 10-fold between AA. For all essential AA (plus serine), inward transport increased with food intake (P<0.04). There were corresponding increases in AA efflux (P<0.05) from the tissues for threonine and the branched-chain AA. Protein synthesis rates estimated from the kinetics of these AA also increased with intake (P<0.02). Rates of inward transport greatly exceeded the amount of AA necessary to support protein retention, but were more similar to rates of protein synthesis. Nutritional or other strategies to enhance AA transport into peripheral tissues are unlikely to increase anabolic responses.