High fat diet promotes experimental colitis by inducing oxidative stress in the colon.

08:00 EDT 14th August 2019 | BioPortfolio

Summary of "High fat diet promotes experimental colitis by inducing oxidative stress in the colon."

Diets high in animal fats are associated with increased risks of inflammatory bowel disease (IBD), but the mechanism remains unclear. In this study we investigated the effect of high fat diet (HFD) on the development of experimental colitis in mice. Relative to mice fed low fat diet (LFD), HFD feeding for 4 weeks increased the levels of triglyceride, cholesterol and free fatty acids in the plasma as well as within the colonic mucosa. In an experimental colitis model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS), mice on 4-week HFD exhibited more severe colonic inflammation and developed more severe colitis compared to the LFD counterparts. HFD feeding resulted in higher production of mucosal pro-inflammatory cytokines, greater activation of the myosin light chain kinase (MLCK) tight junction regulatory pathway, and greater increases in mucosal barrier permeability in mice following TNBS induction. HFD feeding also induced gp91, a NADPH oxidase subunit, and promoted reactive oxygen species (ROS) production in both colonic epithelial cells and lamina propria cells. In HCT116 cell culture, palmitic acid or palmitic acid and TNF-α combination markedly increased ROS production and induced the MLCK pathway, and these effects were markedly diminished in the presence of a ROS scavenger. Taken together, these data suggest that HFD promotes colitis by aggravating mucosal oxidative stress, which rapidly drives mucosal inflammation and increases intestinal mucosal barrier permeability.


Journal Details

This article was published in the following journal.

Name: American journal of physiology. Gastrointestinal and liver physiology
ISSN: 1522-1547


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A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).

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