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Front Physiol. 2017 Jul 24;8:487. doi: 10.3389/fphys.2017.00487. eCollection 2017.

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

Author information

1
Department of Environmental Health Science, University of GeorgiaAthens, GA, United States.
2
Department of Environmental Sciences and Engineering, University of North Carolina at Chapel HillChapel Hill, NC, United States.
3
Department of Population Health and Pathobiology, North Carolina State UniversityRaleigh, NC, United States.

Abstract

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.

KEYWORDS:

artificial sweetener; gut microbiota; inflammation; metabolomics; sucralose

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