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Colitis is an inflammatory bowel disease characterized by inflammation of the colon, accompanied by diarrhea and weight loss. It is caused by a combination of genetic and environmental factors and is more common among people who adhere to a Western dietary pattern high in simple sugars. New research demonstrates how consumption of simple sugars may alter the composition of the gut microbiota in a way that promotes inflammation and disease.
Akkermansia muciniphila (A. muciniphila) is a bacterial species commonly found in the human gut. It degrades mucin, a type of gelatinous protein produced by the intestines to maintain a barrier between the cells that line the gut and the gut microbiota. People with obesity and metabolic disease often have less A. muciniphila in their guts, leading many to explore this species as a probiotic for a number of conditions. However, dietary imbalances can cause A. muciniphila to damage the gut barrier integrity and induce inflammation.
The authors of the study first used a model of colitis that mimics environmental exposure to toxins and then replicated these results in a second model of colitis that mimics genetic susceptibility to colitis. They fed mice a diet providing 10 percent glucose by weight (similar to the sugar content of sugar-sweetened soda) or a normal diet for one week prior to the development of colitis. Mice on the high glucose diet exhibited worse colitis severity, including more diarrhea and weight loss. Mice who continued to consume a high glucose diet after developing colitis continued to experience more severe symptoms.
Through a number of intricate experiments, the authors determined that a high sugar diet increased the number of mucin-degrading bacteria such as A. muciniphila and Bacteroides fragilis. When given antibiotics (which destroy gut bacteria, including mucin-degrading species), glucose-treated mice exhibited less inflammation and less severe colitis symptoms. Finally, when genetically susceptible mice were given a fecal microbiota transplant from glucose-fed healthy mice, they developed more severe colitis, demonstrating the ability to transmit risk from one mouse to another.
This study provides new information about the effects of dietary sugars on colitis severity. The authors provided a wealth of data from a series of well-controlled experiments in mice; however, they noted that the microbiota of mice and humans are very different and clinical studies are needed to confirm these results.
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