191 Early weaning in pigs induces long-term alterations in intestinal nutrient transporter function and expression partially via beta adrenergic enteric neural receptors

Abstract

Abstract Early weaning (EW) has negative impacts on performance and health that persist from wean-to-finish. The mechanisms linking EW and lifetime performance reductions are poorly understood. The objective of this study was to investigate whether EW influences the long-term development of intestinal epithelial nutrient transporter function and expression and the potential mechanisms. Yorkshire gilts were split-weaned from their sows at 15 d (EW) or 28 d of age (Late Weaning; LW) and transferred to an on-site nursery room. All pigs received the same diets in a standard phase feeding program and were euthanized at 75 d of age. Mid-jejunum and distal ileum were mounted on Ussing chambers to evaluate Na+-dependent glucose and amino acid (AA) transporter function, measured as nutrient-induced changes in short circuit current (Isc). EW gilts exhibited reduced capacity for electrogenic transport of glucose (by ~30%; P < 0.05) and glutamate, glutamine, and alanine by (~ 30–35%; P < 0.05), compared with LW pigs. In contrast, jejunal and ileal lysine transporter function was upregulated (by 110% and 25%, respectively; P < 0.05) in EW pigs. Epithelial expression for glucose transporter (SGLT1) was reduced (P < 0.05) while glucose/fructose transporter (GLUT2), fructose transporter (GLUT5) and lysine transporters (B0AT1, CAT1, and ATB0, +) were enhanced in the EW jejunum. No differences observed in villus morphology between EW and LW pigs. Pretreatment of ileal mucosa on Ussing chambers with the Na+ channel blocker (Tetrodotoxin) or the β-adrenergic receptor blocker (Propranolol) augmented glucose, lysine and alanine transporter function in EW but not LW pigs. Together, these data show that EW in gilts induces lasting and divergent alterations in intestinal nutrient transporter function and expression which is mediated in part by the enteric nervous system and β-adrenergic receptor pathways. These new findings may explain why EW pigs exhibit lasting deleterious impacts on performance. Further mechanism-based investigations could reveal new targets for optimizing performance in EW pigs throughout the production lifespan.