Research ArticleColitis

Dietary simple sugars alter microbial ecology in the gut and promote colitis in mice

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Science Translational Medicine  28 Oct 2020:
Vol. 12, Issue 567, eaay6218
DOI: 10.1126/scitranslmed.aay6218

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Harmful sweetness

Inflammatory bowel diseases (IBDs) include multiple disorders characterized by chronic gastrointestinal inflammation. Although the etiology of these diseases is mostly unknown, Western diet and lifestyle seem to be associated with higher IBD incidence. Here, Khan et al. studied the effect of high-sugar diet on colitis in rodent models and showed that a diet high in simple sugars aggravated colitis in mouse models when administered before or after colitis induction. The effect was mediated by alteration of gut microbiota, with an increase of mucolytic bacteria that facilitated gut mucus barrier degradation. The results suggest that high-sugar diet might promote gut microbiota dysfunction and IBD development.

Abstract

The higher prevalence of inflammatory bowel disease (IBD) in Western countries points to Western diet as a possible IBD risk factor. High sugar, which is linked to many noncommunicable diseases, is a hallmark of the Western diet, but its role in IBD remains unknown. Here, we studied the effects of simple sugars such as glucose and fructose on colitis pathogenesis in wild-type and Il10−/− mice. Wild-type mice fed 10% glucose in drinking water or high-glucose diet developed severe colitis induced by dextran sulfate sodium. High-glucose–fed Il10−/− mice also developed a worsened colitis compared to glucose-untreated Il10−/− mice. Short-term intake of high glucose or fructose did not trigger inflammatory responses in healthy gut but markedly altered gut microbiota composition. In particular, the abundance of the mucus-degrading bacteria Akkermansia muciniphila and Bacteroides fragilis was increased. Consistently, bacteria-derived mucolytic enzymes were enriched leading to erosion of the colonic mucus layer of sugar-fed wild-type and Il10−/− mice. Sugar-induced exacerbation of colitis was not observed when mice were treated with antibiotics or maintained in a germ-free environment, suggesting that altered microbiota played a critical role in sugar-induced colitis pathogenesis. Furthermore, germ-free mice colonized with microbiota from sugar-treated mice showed increased colitis susceptibility. Together, these data suggest that intake of simple sugars predisposes to colitis and enhances its pathogenesis via modulation of gut microbiota in mice.

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