Moderate Alcohol Consumption Inhibits Sodium-Dependent Glutamine Co-Transport in Rat Intestinal Epithelial Cells in Vitro and Ex Vivo

• Main Authors: Molly Butts, Raja Singh Paulraj, Jennifer Haynes, Subha Arthur, Soudamani Singh, Uma Sundaram
• Format: Article
• Language: English
• Published: MDPI AG 2019-10-01
• Series: Nutrients
• Subjects: ethanol; enterocyte nutrient absorption; sodium-dependent nutrient co-transport; b0at1
• Online Access: https://www.mdpi.com/2072-6643/11/10/2516

Malnutrition is present in chronic alcoholics. However, how moderate alcohol consumption affects the absorption of nutrients like glutamine has not been investigated. Glutamine, an amino acid, is vital to gastrointestinal health. Glutamine is absorbed via sodium-dependent glutamine co-transport (B0AT1; <i>SLC6A19</i>) along the brush border membrane of absorptive villus cells. Rat intestinal epithelial cells (IEC-18) and sixteen-week-old Sprague Dawley rats were administered the equivalent of a 0.04% blood alcohol content of ethanol (8.64 mM; 2 g/kg) to investigate the effect of moderate alcohol on sodium-glutamine co-transport. Sodium-dependent ³H-glutamine uptakes were performed to measure B0AT1 activity. Inorganic phosphate was measured as a function of Na-K-ATPase activity. Protein expression was analyzed by immunohistochemical and Western blot analysis. Ethanol significantly inhibited sodium-dependent glutamine absorption and Na-K-ATPase activity in enterocytes in vitro and ex vivo. Kinetic studies suggested that the mechanism of inhibition was due to decreased maximal rate of uptake (<i>V_max</i>) of the B0AT1 co-transporter, corresponding to decreased B0AT1 protein expression and secondary to an inhibited sodium-gradient at the cellular level in vitro and ex vivo. In all, moderate ethanol significantly inhibited glutamine absorption at the level of decreased B0AT1 expression at the brush border membrane and a reduced sodium gradient, which may contribute to malnutrition present in chronic alcoholics.