High fructose diet found to exacerbate inflammatory bowel disease
According to the US-based Centers for Disease Control and Prevention (CDC), the number of adults receiving an inflammatory bowel disease (IBD) diagnosis in the country each year increased from 2 million in 1999 to 3 million in 2015. New research suggests that this increase of IBD may be due to higher fructose (refined sugar) consumption in the US in recent times and changes in gut bacteria, which worsens the effect. IBD includes conditions such as ulcerative colitis and Crohn’s disease.
Dr. David Montrose and his colleagues at Weill Cornell Medicine in New York City sought to investigate whether fructose worsens inflammation in three different mouse models of IBD and if changes in the community of microorganisms (microbiota) living in the gut mediate these inflammatory effects.
In the first model, which uses a chemical called dextran sodium sulfate to provoke the kind of inflammatory response that occurs in IBD, a high fructose diet was seen to increase the severity of inflammation while a high glucose diet did not.
The second model involved infecting mice with a bacterium called Citrobacter rodentium, which also mimics the inflammation that characterises IBD. Feeding these mice lots of fructose promoted the growth of the bacteria and worsened inflammation.
Finally, in a third, genetic model of the disease which recreates an immune response that can make some people more susceptible to inflammation of the colon, eating large amounts of fructose was seen to exacerbate and prolong colon inflammation in the animals.
Along with this, the researchers noted several differences due to the changes in gut microbiota: transplants of faecal material from mice fed a high fructose diet exacerbated inflammation in otherwise healthy mice that received them; the layer of mucus protecting the cells that line the colon of mice fed a high fructose diet was found to have thinned and left harmful bacteria in direct contact with the cells; and the high fructose diet also changed the prevalence of several species of bacteria living in the gut, boosting populations of a species known to degrade mucus and is linked to inflammation of the colon.
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