L-Tryptophan Differentially Regulated Glucose and Amino Acid Transporters in the Small Intestine of Rat Challenged with Lipopolysaccharide

SIMPLE SUMMARY: This study aimed to test the hypothesis that L-tryptophan (Trp) modulates lipopolysaccharide (LPS)-induced changes in glucose and amino acid (AA) transport in the rat jejunum in a transporter-dependent manner. Rats were fed Trp in drinking water for 7 days and were intraperitoneally injected with LPS once. Jejunum samples isolated from rats were used for the determination of glucose and AA transport using an Ussing chamber and the expression of related transporters. We found that LPS-induced gut inflammation reduced glucose and AA transport in the jejunum of the rats. Tryptophan supplementation alleviated the LPS-induced downregulation of the expression of the glucose transporter SGLT1, the AA transporters solute carrier family 38 member 2 (SNAT2) and solute carrier family 7 member 8 (LAT2), as well as ATPase Na(+)/K(+) transporting subunit alpha 2 (ATP1A2); however, it increased the LPS-induced upregulation of acidic AA transporter solute carrier family 1 member 1 (EAAT3) expression. ABSTRACT: Tryptophan (Trp) has been shown to improve the growth and gut function of weaned piglets. Whether the growth-promoting effect of Trp is due to the improvement in nutrient transport and absorption during weaning or under conditions of inflammation has not been fully characterized. The objective of this study was to determine the effects of Trp on lipopolysaccharide (LPS)-induced changes in glucose and amino acid (AA) transport in the rat jejunum. Twenty-four 7-week-old Sprague Dawley rats were randomly divided into one of three groups: control, LPS, and Trp + LPS. Rats were supplemented with 0 or 0.1 mg Trp per gram body weight/d in drinking water for 7 days and were intraperitoneally injected with LPS (5 mg/kg BW) on day 8. After 24 h, rats were sacrificed, and jejunum samples were isolated for the analysis of glucose and AA transport using an Ussing chamber and the expression of glucose and AA transporters. The results showed that Trp alleviated the LPS-induced increase in jejunal permeability (p < 0.05) and decrease in changes in the short-circuit current of glucose, arginine, glutamine, glutamate, glycine, histidine, leucine, lysine, taurine, threonine, and Trp (p < 0.05). Trp reversed (p < 0.05) the LPS-induced downregulation of expression of the glucose transporter SGLT1 and AA transporters solute carrier family 38 member 2 (SNAT2) and solute carrier family 7 member 8 (LAT2), as well as ATPase Na(+)/K(+) transporting subunit alpha 2 (ATP1A2). However, Trp increased (p < 0.01) the LPS-induced upregulation of acidic AA transporter solute carrier family 1 member 1 (EAAT3) expression. The above findings may help to develop nutritional interventions for the differential targeting of gut nutrient transporters, aiming to improve gut function and health in the presence of inflammation in both humans and animals.