Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.814238
Title: Artificial sweeteners negatively impact gut epithelium and microflora
Author: Shil, Aparna
ISNI:       0000 0004 9353 1061
Awarding Body: Anglia Ruskin University
Current Institution: Anglia Ruskin University
Date of Award: 2020
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Abstract:
Artificial sweeteners (AS) are synthetic sugar substitutes which are commonly consumed in the diet for their low-calorie profile. Recent studies have indicated considerable health risks; consumption of AS linked to metabolic derangements and gut microflora perturbations. Despite these studies, there is still limited data on how AS affects intestinal epithelium or impacts the commensal microbiota to cause pathogenicity. Furthermore, it is not well-understood whether the orphan G-protein coupled receptor (T1R2/3), which binds AS, is responsible for these health risks. The current in vitro study sought to investigate the role of commonly consumed AS on: intestinal epithelial cell function, gut bacterial metabolism and pathogenicity, and gut epithelium-microbiota interactions, using models of the intestinal epithelium (Caco-2) and microflora (Escherichia coli NCTC10418 and Enterococcus faecalis ATCC19433). To address these aims, Caco-2 and model gut bacteria (MGB) were exposed to different concentrations of the AS; saccharin, sucralose, aspartame and neotame; and various in vitro studies were performed. Saccharin, aspartame and neotame decreased cell viability at physiological concentrations, whilst all increased permeability across the intestinal epithelial monolayer at either physiological or sub-physiological concentrations. Interestingly, these damaging effects were mediated through a T1R2/3-independent pathway. In the MGB studied, AS exposure had no impact on metabolic parameters, but increased pathogenicity of E. coli as measured by biofilm formation. Furthermore, AS differentially increased adhesion and invasion of MGB into Caco-2 cells, which is indicative of a pathogenic response. Interestingly, inhibition of sweet sensing attenuated these pathogenic effects. These findings suggest that AS negatively impact gut physiology by directly damaging the intestinal epithelium and by increasing the pathogenicity of MGB. These outputs are linked with inflammation and potential development of metabolic diseases such as diabetes. Further investigations are, however, needed to utilise these findings to prevent AS-induced intestinal damage. Since AS consumption is so high in the population, understanding how this food additive affects gut health and how these damaging effects can be ameliorated is vital.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.814238  DOI: Not available
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