A new study in Frontiers in Nutrition indicates that artificial sweetener neotame may negatively regulate the intestinal epithelium directly through T1R3-signaling and indirectly through pathogenic changes to model gut bacteria. While recent studies have indicated considerable health risks associated with the consumption of artificial sweeteners, there hasn’t been as much study on neotame, which has been used in foodstuffs since FDA approval in 2002. What follows are the results, direct from the study, which is part of the research topic, Noncaloric Artificial Sweeteners and their Impact On Human Health.
Results: Our findings show that neotame causes intestinal epithelial cell apoptosis and death with siRNA knockdown of T1R3 expression significantly attenuating the neotame-induced loss to cell viability. Similarly, neotame exposure results in barrier disruption with enhanced monolayer leak and reduced claudin-3 cell surface expression through a T1R3-dependent pathway. Using the gut bacteria models, E. coli and E. faecalis, neotame significantly increased biofilm formation and metabolites of E. coli, but not E. faecalis, reduced Caco-2 cell viability. In co-culture studies, neotame exposure increased adhesion capacity of E. coli and E. faecalis onto Caco-2 cells and invasion capacity of E. coli. Neotame-induced biofilm formation, E.coli-specific Caco-2 cell death, adhesion and invasion was identified to be meditated through a taste-dependent pathway.