PSVI-4 Serum Metabolomic Characterization of Birth Weight and Neonatal Nutrient Restriction on Piglet Growth and Development

Abstract

Abstract The objective was to characterize developmental differences in low birth weight (LBW) and normal birth weight (NBW) piglets with or without nutrient restriction using serum metabolomic profile analysis. After farrowing, 112 piglets were selected as LBW (1.22 ± 0.28 kg) or NBW (1.70 ± 0.27 kg) and were categorized to receive normal nutrition (NN) or restricted nutrition (RN - 6 h/day no suckling) until d 28 when the pigs were weaned onto a common diet until d 56. Blood samples were taken on d 28 and d 56 (n=8 pigs/treatment) and were analyzed using quantitative metabolomics via a combination of direct injection mass spectrometry with a reverse-phase LC-MS/MS custom assay (TMIC prime). Data were normalized using logarithmic transformation and auto-scaling. Partial least squares discriminant analysis (PLS-DA) was carried out to further explore the differential metabolites among the treatments (metaboanalyst.ca) with an integrated enrichment and pathway topography analysis. The results suggest that at d 28, LBW piglets had decreased metabolites associated with fatty acid oxidation, glycolysis and TCA cycle metabolites, and essential amino acids such as valine, leucine, arginine. These indicate a decrease utilization of gluconeogenic, and TCA cycle pathways compared with the NBW group. On d 56, LBW piglets had increased utilization of fatty acids, exhibited by increased production of serum acetoacetate, B-hydroxybutyrate, glycerol, compared with NBW. Additionally, the LBW piglets had decreased glucose utilization, pyruvate, succinate, citrate, a-ketoglutaric acid, and lactate compared with the NBW piglets. Due to low utilization of glycolysis and the TCA cycle, associated amino acids were less in LBW piglets, except for a increased glycerol which may indicate impairments in glucose tolerance. In summary, LBW piglets appear to have more metabolic deficiencies in early life, which is not resolved with nutrition in early life, but may be responsive to a tailored nutritional intervention post-weaning.