Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome

By B. Chassaing, Omry Koren, Julia Goodrich, Angela C. Poole, S. Srinivasan, Ruth E. Ley, A. Gewirtz. Nature, 2015

1,790 citations recorded by the source corpus.

The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota–host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome. A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine. Thus, agents that disrupt mucus–bacterial interactions might have the potential to promote diseases associated with gut inflammation. Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host–microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.

Subfields: Gastroenterology, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/acb0d2387b1a8f731d7da7ac5f6732d543802491

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Citations in the corpus

Ultra-processed food intake and risk of cardiovascular disease: prospective cohort study (NutriNet-Santé) (2019, background): “32 Carrageenan, used as a food additive for its thickening properties, might lead to glucose intolerance, insulin resistance, and inhibition of insulin signalling, as shown in a study on cell and animal models.”
The Western Diet–Microbiome-Host Interaction and Its Role in Metabolic Disease (2018, neutral): “These data are shedding some eagerly awaited light on the mechanisms of leptin resistance, and can provide an explanation for the imbalance in energy intake and energy expenditure coinciding with gut inflammation as observed in mice [29].”
A dietary fiber-deprived gut microbiota degrades the colonic mucus barrier and enhances pathogen susceptibility (2016, positive): “However, measurements of three additional host parameters provided support for altered host responses in the face of mucus erosion: the first was fecal lipocalin—a neutrophil protein that binds bacterial siderophores and is associated with low-grade inflammation (Chassaing et al., 2015)—that was inc”
Metabolic Control of Longevity. (2016, background): “Moreover, dietary emulsifiers and other additives used in the food industry have a negative impact on the gut microbiota, hence promoting intestinal inflammation and metabolic syndrome (at least in mice) (Chassaing et al., 2015).”