4.7 Article

A Mediterranean-like fat blend protects against the development of severe colitis in the mucin-2 deficient murine model

期刊

GUT MICROBES
卷 14, 期 1, 页码 -

出版社

TAYLOR & FRANCIS INC
DOI: 10.1080/19490976.2022.2055441

关键词

Colitis; ulcerative colitis; inflammation; dietary fat; mediterranean diet; mucin 2; diet; nutrition; bacteriome

资金

  1. Canadian Institutes of Health Research Frederick Banting and Charles Best Canada Graduate Doctoral Award
  2. Canadian Association of Gastroenterology PhD Studentship Award
  3. Crohn's and Colitis Canada
  4. NSERC
  5. Natural Sciences and Engineering Research Council of Canada

向作者/读者索取更多资源

There is a growing awareness of the interaction between diet, gut microbiota, and the immune system in the development of inflammatory bowel disease (IBD). High-fat diets have been shown to exacerbate IBD, while the fat blend found in the Mediterranean diet (MD) may have protective effects. A study in mice found that a diet mimicking the MD fat blend reduced disease activity and inflammation, and improved metabolic parameters in a mouse model of IBD.
There is a growing appreciation that the interaction between diet, the gut microbiota and the immune system contribute to the development and progression of inflammatory bowel disease (IBD). A mounting body of scientific evidence suggests that high-fat diets exacerbate IBD; however, there is a lack of information on how specific types of fat impact colitis. The Mediterranean diet (MD) is considered a health-promoting diet containing approximately 40% total fat. It is not known if the blend of fats found in the MD contributes to its beneficial protective effects. Mice deficient in the mucin 2 gene (Muc 2(-/-)) were weaned to 40% fat, isocaloric, isonitrogenous diets. We compared the MD fat blend (high monounsaturated, 2:1 n-6:n-3 polyunsaturated and moderate saturated fat) to diets composed of corn oil (CO, n-6 polyunsaturated-rich), olive oil (monounsaturated-rich) or milk fat (MF, saturated-rich) on spontaneous colitis development in Muc2(-/-) mice. The MD resulted in lower clinical and histopathological scores and induced tolerogenic CD103+ CD11b+ dendritic, Th22 and IL-17+ IL-22+ cells necessary for intestinal barrier repair. The MD was associated with beneficial microbes and associated with higher cecal acetic acid levels negatively correlated with colitogenic microbes like Akkermansia muciniphila. In contrast, CO showed a higher prevalence of mucin-degraders including A. muciniphila and Enterobacteriaceae, which have been associated with colitis. A dietary blend of fats mimicking the MD, reduces disease activity, inflammation-related biomarkers and improves metabolic parameters in the Muc2(-/-) mouse model. Our findings suggest that the MD fat blend could be incorporated into a maintenance diet for colitis.

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