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Moderate Alcohol Consumption Inhibits Sodium-Dependent Glutamine Co-Transport in Rat Intestinal Epithelial Cells in Vitro and Ex Vivo
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 (B0A...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6835445/ https://www.ncbi.nlm.nih.gov/pubmed/31635319 http://dx.doi.org/10.3390/nu11102516 |
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author | Butts, Molly Singh Paulraj, Raja Haynes, Jennifer Arthur, Subha Singh, Soudamani Sundaram, Uma |
author_facet | Butts, Molly Singh Paulraj, Raja Haynes, Jennifer Arthur, Subha Singh, Soudamani Sundaram, Uma |
author_sort | Butts, Molly |
collection | PubMed |
description | 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; SLC6A19) 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 (3)H-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 (V(max)) 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. |
format | Online Article Text |
id | pubmed-6835445 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-68354452019-11-25 Moderate Alcohol Consumption Inhibits Sodium-Dependent Glutamine Co-Transport in Rat Intestinal Epithelial Cells in Vitro and Ex Vivo Butts, Molly Singh Paulraj, Raja Haynes, Jennifer Arthur, Subha Singh, Soudamani Sundaram, Uma Nutrients Article 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; SLC6A19) 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 (3)H-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 (V(max)) 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. MDPI 2019-10-18 /pmc/articles/PMC6835445/ /pubmed/31635319 http://dx.doi.org/10.3390/nu11102516 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Butts, Molly Singh Paulraj, Raja Haynes, Jennifer Arthur, Subha Singh, Soudamani Sundaram, Uma Moderate Alcohol Consumption Inhibits Sodium-Dependent Glutamine Co-Transport in Rat Intestinal Epithelial Cells in Vitro and Ex Vivo |
title | Moderate Alcohol Consumption Inhibits Sodium-Dependent Glutamine Co-Transport in Rat Intestinal Epithelial Cells in Vitro and Ex Vivo |
title_full | Moderate Alcohol Consumption Inhibits Sodium-Dependent Glutamine Co-Transport in Rat Intestinal Epithelial Cells in Vitro and Ex Vivo |
title_fullStr | Moderate Alcohol Consumption Inhibits Sodium-Dependent Glutamine Co-Transport in Rat Intestinal Epithelial Cells in Vitro and Ex Vivo |
title_full_unstemmed | Moderate Alcohol Consumption Inhibits Sodium-Dependent Glutamine Co-Transport in Rat Intestinal Epithelial Cells in Vitro and Ex Vivo |
title_short | Moderate Alcohol Consumption Inhibits Sodium-Dependent Glutamine Co-Transport in Rat Intestinal Epithelial Cells in Vitro and Ex Vivo |
title_sort | moderate alcohol consumption inhibits sodium-dependent glutamine co-transport in rat intestinal epithelial cells in vitro and ex vivo |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6835445/ https://www.ncbi.nlm.nih.gov/pubmed/31635319 http://dx.doi.org/10.3390/nu11102516 |
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