Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 7, 2010
Publication Date: August 1, 2010
Citation: Oliver, W.T., Miles, J.R. 2010. A Low-fat Liquid Diet Increases Protein Accretion and Alters Cellular Signaling for Protein Synthesis in 10-day-old Pigs. Journal of Animal Science. 88(8):2576-2584. Interpretive Summary: Dramatic improvements have been made in the postweaning growth performance in swine. However, attempts to improve growth rate during the nursing phase of production have largely been unsuccessful. The young pig has a high propensity for muscle growth. This is driven largely by high rates of protein synthesis, which reduces dramatically as the animal ages. Improvements in growth performance and body composition in the neonatal pig has the potential to reduce days to market and increase the carcass merit of pigs. In addition, the identification of the characteristics of the immature muscle that is responsible for the high rate of muscle protein synthesis and accretion will provide a rational underpinning for the development of new approaches for promoting the accretion of muscle mass throughout the production cycle. Research conducted at the U.S. Meat Animal Research Center determined that feeding a low-fat liquid diet to pigs weaned from the sow at 10 days of age increases feed intake to meet their energy needs, while maintaining growth performance. In addition, 10-day-old pigs consuming a low-fat liquid diet have altered cellular signaling for protein synthesis leading to increased protein deposition and decreased fat deposition compared to pigs consuming a high-fat diet.
Technical Abstract: Previous research shows that neonatal pigs respond to decreases in energy density of liquid diets with increased feed intake, resulting in similar performance to pigs fed a more energy dense diet. The objective of this experiment was to determine if a high-(25%, HF) or low-fat (2%, LF) liquid diet affects nutrient accretion rate and select proteins involved in energy homeostasis and protein synthesis in early-weaned pigs. Forty-eight pigs, with an initial body weight of 3,637 ± 85 g, were weaned from the sow at 10 d of age and utilized in a randomized complete block design. Pigs were blocked by weight, and then assigned to pens (8 pigs/pen). Diets were formulated to provide a constant AA:ME ratio and were fed for a duration of 10 d. Pigs were killed at d 10, 15, and 20 of age, at which time blood and longissimus dorsi were collected, and carcasses were prepared for body composition analysis. Blood was analyzed for plasma urea nitrogen (PUN) and NEFA. Longissimus dorsi was analyzed via western immunoblot for mammalian target of rapamycin (mTOR) and adenosine 5’ monophosphate-activated protein kinase (AMPK) phosphorylation. Pigs gained 347 ± 11 g/d, which resulted in an ending body weight of 6,858 ± 135 g, regardless of dietary treatment (P > 0.49). Pigs fed the LF diet consumed 25% more milk than pigs fed the HF diet (2,853 ± 86 vs. 2,269 ± 79 g dry feed•pen-1•d-1; P < 0.01), which resulted in similar calculated ME intakes between dietary treatments (9.9 ± 0.2 vs. 10.5 ± 0.2 Mcal•pen-1•d-1; P > 0.5). Feed conversion (gain:feed) was 24% higher in HF compared to LF fed pigs (P < 0.01). Circulating NEFA (138 ± 21 vs. 40 ± 14 uEq/L; P < 0.01) and PUN (17.7 ± 0.8 vs. 3.0 ± 0.6 mM; P < 0.01) concentrations were lower in LF pigs compared to HF pigs after 10 d of dietary treatments. Pigs consuming the LF diet had a 21% increase in protein accretion (50.5 ± 2.8 vs. 61.2 ± 2.8 g/d; P < 0.04) and a 71% reduced lipid accretion rate (28.8 ± 2.0 vs. 8.3 ± 2.3 g/d; P < 0.001). Phosphorylation of AMPK was 29% lower (P < 0.03) in LF pigs compared to HF pigs, while mTOR phosphorylation was increased by 37% in LF pigs (P < 0.01). Thus, we conclude that feeding a LF liquid diet to pigs weaned from the sow at 10 d of age increases feed intake to regulate energy intake while maintaining growth performance. In addition, 10-d-old pigs consuming a liquid LF diet have increased protein deposition by a mechanism mediated through AMPK and mTOR.