A revised model of energy transactions and body composition in sheep.

A mechanistic, dynamic model was developed to calculate body composition in growing lambs by calculating heat production (HP) internally from energy transactions within the body. The model has a fat pool (f) and three protein pools: visceral (v), nonvisceral (m), and wool (w). Heat production is calculated as the sum of fasting heat production, heat of product formation (HrE), and heat associated with feeding (HAF). Fasting heat production is represented as a function of visceral and nonvisceral protein mass. Heat associated with feeding (HAF) is calculated as ((1 - km) x MEI), where km is partial efficiency of ME use for maintenance, and MEI = metabolizable energy intake) applies at all levels above and below maintenance. The value of km derived from data where lambs were fed above maintenance was 0.7. Protein change (dp/dt) is the sum of change in the m, v, and w pools, and change in fat is equal to net energy available for gain minus dp/dt. Heat associated with a change in body composition (HrE) is calculated from the change in protein and fat with estimated partial efficiencies of energy use of 0.4 and 0.7 for protein and fat, respectively. The model allows for individuals to gain protein while losing fat or vice versa. When evaluated with independent data, the model performed better than the current Australian feeding standards (Freer et al., 2007) for predicting protein gain in the empty body but did not perform as well as for gain of fat and fleece-free empty body weight. Models performed similarly for predicting clean wool growth. By explicit representation of the major energy using processes in the body, and through simplification of the way body composition is computed in growing animals, the model is more transparent than current feeding systems while achieving similar performance. An advantage of this approach is that the model has the potential for wider applicability across different growth trajectories and can explicitly account for the effects of systematic changes on energy transactions, such as the effects of selective breeding, growth manipulation, or environmental changes.

Based on prior work by Oltjen et al. (2006), a revised dynamic, mechanistic model was developed to improve the prediction of the composition of protein and fat in the body of growing ruminants. The revised model calculates heat production (HP) internally as a function of fasting HP, heat associated with feeding, and HP from changes in fat and protein within the body. Heat associated with product formation is calculated from changes in body protein and fat, with separate efficiencies for each, while heat associated with feeding is a constant proportion of metabolizable energy intake and applies at all levels of feeding above and below maintenance. When evaluated against novel data, the revised model performed similarly to current Australian feeding standards (Freer et al., 2007) Unlike the Freer model, the revised model captures variation in HP arising from feed as well as gain of protein and fat. The revised model explicitly represents protein in the body as two pools with markedly different rates of energy expenditure, improving representation of the underlying biology compared to current feeding systems. This provides a more flexible way to predict energy requirements and body composition in growing animals while achieving similar performance to current feeding systems.

Effects of dietary energy density and supplemental rumen undegradable protein on intake, viscera, and carcass composition of lambs recovering from nutritional restriction.

Variation in nutrition is a key determinant of growth, body composition, and the ability of animals to perform to their genetic potential. Depending on the quality of feed available, animals may be able to overcome negative effects of prior nutritional restriction, increasing intake and rates of tissue gain, but full compensation may not occur. A 2 × 3 × 4 factorial serial slaughter study was conducted to examine the effects of prior nutritional restriction, dietary energy density, and supplemental rumen undegradable protein (RUP) on intake, growth, and body composition of lambs. After an initial slaughter (n = 8), 124 4-mo-old Merino cross wethers (28.4 ± 1.8 kg) were assigned to either restricted (LO, 500 g/d) or unrestricted (HI, 1500 g/d) intake of lucerne and oat pellets. After 8 wk, eight lambs/group were slaughtered and tissue weights and chemical composition were measured. Remaining lambs were randomly assigned to a factorial combination of dietary energy density (7.8, 9.2, and 10.7 MJ/kg DM) and supplemental RUP (0, 30, 60, and 90 g/d) and fed ad libitum for a 12- to 13-wk experimental period before slaughter and analysis. By week 3 of the experimental period, lambs fed the same level of energy had similar DMI (g/d) and MEI (MJ/d) (P > 0.05), regardless of prior level of nutrition. Restricted-refed (LO) lambs had higher rates of fat and protein gain than HI lambs (P < 0.05) but had similar visceral masses (P > 0.05). However, LO lambs were lighter and leaner at slaughter, with proportionally larger rumens and livers (P < 0.05). Tissue masses increased with increasing dietary energy density, as did DMI, energy and nitrogen (N) retention (% intake), and rates of protein and fat gain (P < 0.05). The liver increased proportionally with increasing dietary energy density and RUP (P < 0.05), but rumen size decreased relative to the empty body as dietary energy density increased (P < 0.05) and did not respond to RUP (P > 0.05). Fat deposition was greatest in lambs fed 60 g/d supplemental RUP (P < 0.05). However, lambs fed 90 g/d were as lean as lambs that did not receive supplement (P0, P > 0.05), with poorer nitrogen retention and proportionally heavier livers than P0 lambs (P < 0.05). In general, visceral protein was the first tissue to respond to increased intake during refeeding, followed by non-visceral protein and fat, highlighting the influence of differences in tissue response over time on animal performance and body composition.

Animal performance is determined by the combined effects of both prior and current nutrition. The present study used a 2 × 3 × 4 factorial to examine the effects of prior feeding level (HI or LO) on subsequent ad-libitum intake of diets varying in energy density (7.8, 9.2, 10.7 MJ/kg DM) and level of supplemental rumen undegradable protein (RUP; 0, 30, 60, and 90g/d). By week 3 of refeeding, LO and HI lambs had similar feed intake, but LO lambs had proportionally more gut and liver tissue and were lighter and leaner at final slaughter. As dietary energy density increased, the rumen became proportionally smaller while the liver became proportionally larger. Liver size increased with increasing RUP, and lambs fed 30 and 60 g/d were fatter than other lambs. However, lambs fed 90 g/d RUP had less fat than other lambs, as the increased energy requirements of a larger liver and of disposing of excess nitrogen appeared to outweigh any nutritional benefits. Understanding how prior nutrition affects current performance, as well as how tissues vary in their response to the same diet, is key to improving our understanding of animal performance and response to change.

Reduced feeding during water deprivation depends on hydration of the gut.

Removal of drinking water at the start of the dark period reduced food intake in freely feeding rats within 45 min. Both first and later meals were smaller during 7.5 h of water deprivation, but meal frequency did not change. Ingestion of a normal-sized meal (3 g) rapidly increased plasma tonicity when drinking water was withheld, but intravenous infusions of hypertonic NaCl causing similar increases in plasma tonicity did not reduce feeding. Feeding during 6 h of water deprivation was restored by slowly infusing the volume of water normally drunk into the stomach, jejunum, or cecum, but not in the vena cava or hepatic portal vein. The infusions did not alter water or electrolyte excretion or affect food intake in rats allowed to drink. We conclude that the inhibition of feeding seen during water deprivation is mediated by a sensor that is located in the gastrointestinal tract or perhaps in the mesenteric veins draining the gut, but not the hepatic portal vein or the liver. In the absence of drinking water, signals from this sensor provoke the early termination of a meal.