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                Figure 2. The effect of Akk on intestinal-related diseases. Administration of Akk or its components to humans or mice can alleviate
                intestinal inflammation, tumors, and functional gastrointestinal diseases, as well as metabolic regulation such as alleviation of obesity,
                insulin resistance, and liver disease. Administering Akk or its components to humans or mice has been shown to reduce intestinal
                inflammation, inhibit tumor growth, and alleviate functional gastrointestinal disorders. Additionally, it contributes to metabolic
                regulation, including the reduction of obesity, improvement of insulin sensitivity, and mitigation of liver disease. Created with
                BioRender.com. Akk: Akkermansia muciniphila.

               consistent with this. Studies on IBD patients showed that compared with healthy people, the relative
               abundance of Akk in the colon was significantly reduced in UC patients, as well as in CD patients [10,22-24] .
               Several experiments on mouse models of colitis also support a beneficial role for Akk in controlling
               intestinal inflammation. For example, a study in 2020 showed that the abundance of Akk was significantly
               reduced in DSS-induced colitis mice . After treatment of DSS-induced colitis mice with secondary bile
                                               [21]
               acid, the abundance of Akk in the feces was significantly increased . Similar results were obtained with
                                                                         [25]
               hyaluronic acid-bilirubin nanomedicine (HABN) treatment . It was also found in an Escherichia coli
                                                                    [26]
               infectious ileitis model that mice overexpressing tryptophan metabolizing enzyme indoleamine 2,3-
               dioxygenase 1 (IDO1) showed remission of inflammation, thickened intestinal mucus layer, and increased
               proportion of Akk compared to control mice . Furthermore, in an intestinal epithelium-specific
                                                         [27]
               autophagy-related protein 5 (ATG5) knockout mouse model, ATG5 deficiency was found to result in a
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