A high-sugar diet rapidly enhances susceptibility to colitis
The aim of this study was to identify the effect of a short-term diet high in sugar on susceptibility to colitis.
Most experimental findings relating to the ‘western diet’ and IBD have focused on high-fat content alone or in combination with high-sugar; thus the isolated effects of dietary refined sugars on enteric microbial composition, luminal milieu, and susceptibility to colitis are not well understood2. Population-based studies have demonstrated an association between intake of refined sugar and artificial sweeteners and increased incidence of IBD7,8,9,10,11,12. In addition, dietary surveys indicate that ~10% of IBD patients feel that “sugary” foods trigger disease flare-ups and worsen severity of their symptoms13,14.
Interestingly, the elevated incidence of IBD associated with a high-sugar diet can be reversed by a diet rich in fiber8. The protective mechanism of dietary fiber is thought to be due in part to the metabolism of carbohydrate polymers into short-chain fatty acids (SCFAs) by specific bacterial populations15. SCFAs, which include butyrate and acetate, are thought to play a role in IBD status which is supported by the fact that depressed levels of SCFAs have been described in the stool of IBD patients16,17,18.
In this study we demonstrate that a two-day exposure to a high-sugar diet rapidly alters gut microbial composition, depletes short chain fatty acids and increases susceptibility to chemically induced colitis. This effect was significantly attenuated through the supplementation of acetate independently of changes in microbial community composition. These findings are consistent with recent literature purporting the risks of a high-sugar diet in the triggering and perpetuation of inflammatory bowel diseases and the protective role of SCFA8,15,31.
The dramatic effect of just two days of a high-sugar diet on microbial function and populations may shed light on the role of diet in triggering disease flares in patients with inflammatory bowel disease. An especially meaningful change in this study included the loss of important SCFA producing microbes belonging to the Lachnospiraceae family. This family is capable of producing numerous SCFAs, including butyrate and acetate32.
A high sugar diet was also associated with an overall decrease in microbial α-diversity compared to chow diet. Community diversity and the interactions between different microbes are crucial in the production of SCFAs33,34. Therefore, the loss of individual microbial groups important in the creation of SCFAs, alongside a loss in overall community α-diversity, may be responsible for the decline in luminal SCFAs seen in a high-sugar diet.
Interestingly, some artificial sweeteners have also been shown to alter gut microbiota and influence host physiological responses35,36,37. A study by Suez et al.36 showed that consumption of saccharin for 5 days in healthy human volunteers resulted in decreased glycemic responses that correlated with alterations in gut microbiota. It remains to be shown however, if short-term intake of sweeteners also increases susceptibility to colitis.
In conclusion, this paper provides mechanistic insight into the epidemiologic findings implicating a high-sugar diet in the triggering and perpetuation of inflammation in patients with inflammatory bowel disease. The results show that a short-term diet high in sugar results in an enhanced intestinal permeability coupled with a more inflammatory monocyte phenotype that results in an increased susceptibility to colonic insults and a lack of ability to repair damage. The findings that acetate alone substantially alleviates the deleterious effects of a high-sugar diet adds to the body of evidence suggesting that SCFAs play a crucial role in the response of the gut to insults and tissue repair.
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