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Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice

Sucralose is the most widely used artificial sweetener, and its health effects have been highly debated over the years. In particular, previous studies have shown that sucralose consumption can alter the gut microbiota. The gut microbiome plays a key role in processes related to host health, such as...

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Autores principales: Bian, Xiaoming, Chi, Liang, Gao, Bei, Tu, Pengcheng, Ru, Hongyu, Lu, Kun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5522834/
https://www.ncbi.nlm.nih.gov/pubmed/28790923
http://dx.doi.org/10.3389/fphys.2017.00487
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author Bian, Xiaoming
Chi, Liang
Gao, Bei
Tu, Pengcheng
Ru, Hongyu
Lu, Kun
author_facet Bian, Xiaoming
Chi, Liang
Gao, Bei
Tu, Pengcheng
Ru, Hongyu
Lu, Kun
author_sort Bian, Xiaoming
collection PubMed
description Sucralose is the most widely used artificial sweetener, and its health effects have been highly debated over the years. In particular, previous studies have shown that sucralose consumption can alter the gut microbiota. The gut microbiome plays a key role in processes related to host health, such as food digestion and fermentation, immune cell development, and enteric nervous system regulation. Inflammation is one of the most common effects associated with gut microbiome dysbiosis, which has been linked to a series of human diseases, such as diabetes and obesity. The aim of this study was to investigate the structural and functional effects of sucralose on the gut microbiota and associated inflammation in the host. In this study, C57BL/6 male mice received sucralose in their drinking water for 6 months. The difference in gut microbiota composition and metabolites between control and sucralose-treated mice was determined using 16S rRNA gene sequencing, functional gene enrichment analysis and metabolomics. Inflammatory gene expression in tissues was analyzed by RT-PCR. Alterations in bacterial genera showed that sucralose affects the gut microbiota and its developmental dynamics. Enrichment of bacterial pro-inflammatory genes and disruption in fecal metabolites suggest that 6-month sucralose consumption at the human acceptable daily intake (ADI) may increase the risk of developing tissue inflammation by disrupting the gut microbiota, which is supported by elevated pro-inflammatory gene expression in the liver of sucralose-treated mice. Our results highlight the role of sucralose-gut microbiome interaction in regulating host health-related processes, particularly chronic inflammation.
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spelling pubmed-55228342017-08-08 Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice Bian, Xiaoming Chi, Liang Gao, Bei Tu, Pengcheng Ru, Hongyu Lu, Kun Front Physiol Physiology Sucralose is the most widely used artificial sweetener, and its health effects have been highly debated over the years. In particular, previous studies have shown that sucralose consumption can alter the gut microbiota. The gut microbiome plays a key role in processes related to host health, such as food digestion and fermentation, immune cell development, and enteric nervous system regulation. Inflammation is one of the most common effects associated with gut microbiome dysbiosis, which has been linked to a series of human diseases, such as diabetes and obesity. The aim of this study was to investigate the structural and functional effects of sucralose on the gut microbiota and associated inflammation in the host. In this study, C57BL/6 male mice received sucralose in their drinking water for 6 months. The difference in gut microbiota composition and metabolites between control and sucralose-treated mice was determined using 16S rRNA gene sequencing, functional gene enrichment analysis and metabolomics. Inflammatory gene expression in tissues was analyzed by RT-PCR. Alterations in bacterial genera showed that sucralose affects the gut microbiota and its developmental dynamics. Enrichment of bacterial pro-inflammatory genes and disruption in fecal metabolites suggest that 6-month sucralose consumption at the human acceptable daily intake (ADI) may increase the risk of developing tissue inflammation by disrupting the gut microbiota, which is supported by elevated pro-inflammatory gene expression in the liver of sucralose-treated mice. Our results highlight the role of sucralose-gut microbiome interaction in regulating host health-related processes, particularly chronic inflammation. Frontiers Media S.A. 2017-07-24 /pmc/articles/PMC5522834/ /pubmed/28790923 http://dx.doi.org/10.3389/fphys.2017.00487 Text en Copyright © 2017 Bian, Chi, Gao, Tu, Ru and Lu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Bian, Xiaoming
Chi, Liang
Gao, Bei
Tu, Pengcheng
Ru, Hongyu
Lu, Kun
Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice
title Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice
title_full Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice
title_fullStr Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice
title_full_unstemmed Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice
title_short Gut Microbiome Response to Sucralose and Its Potential Role in Inducing Liver Inflammation in Mice
title_sort gut microbiome response to sucralose and its potential role in inducing liver inflammation in mice
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5522834/
https://www.ncbi.nlm.nih.gov/pubmed/28790923
http://dx.doi.org/10.3389/fphys.2017.00487
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