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      Considering gut microbiota in treatment of type 2 diabetes mellitus

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      Author(s): ,
      Publication date (Electronic, pub):
      Publication date (Electronic, collection):
      Journal: Gut Microbes
      Publisher: Taylor & Francis
      Keywords: Diabetes, inflammation, microbiota metformin, dietary fiber

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          ABSTRACT

          Advances in the understanding of the pathogenesis of type 2 diabetes mellitus (T2D) have revealed a role for gut microbiota dysbiosis in driving this disease. This suggests the possibility that approaches to restore a healthy host–microbiota relationship might be a means of ameliorating T2D. Indeed, recent studies indicate that many currently used treatments for T2D are reported to impact gut microbiota composition. Such changes in gut microbiota may mediate and/or reflect the efficacy of these interventions. This article outlines the rationale for considering the microbiota as a central determent of development of T2D and, moreover, reviews evidence that impacting microbiota might be germane to amelioration of T2D, both in terms of understanding mechanisms that mediate efficacy of exiting T2D therapies and in developing novel treatments for this disorder.

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          Improvement of Insulin Sensitivity after Lean Donor Feces in Metabolic Syndrome Is Driven by Baseline Intestinal Microbiota Composition

          Ruud S Kootte, Evgeni Levin, Jarkko Salojärvi … (2017)
          The intestinal microbiota has been implicated in insulin resistance, although evidence regarding causality in humans is scarce. We therefore studied the effect of lean donor (allogenic) versus own (autologous) fecal microbiota transplantation (FMT) to male recipients with the metabolic syndrome. Whereas we did not observe metabolic changes at 18 weeks after FMT, insulin sensitivity at 6 weeks after allogenic FMT was significantly improved, accompanied by altered microbiota composition. We also observed changes in plasma metabolites such as γ-aminobutyric acid and show that metabolic response upon allogenic FMT (defined as improved insulin sensitivity 6 weeks after FMT) is dependent on decreased fecal microbial diversity at baseline. In conclusion, the beneficial effects of lean donor FMT on glucose metabolism are associated with changes in intestinal microbiota and plasma metabolites and can be predicted based on baseline fecal microbiota composition.
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            Fiber-Mediated Nourishment of Gut Microbiota Protects against Diet-Induced Obesity by Restoring IL-22-Mediated Colonic Health

            Jun Zou, Benoit Chassaing, Vishal Singh … (2018)
            Dietary supplementation with fermentable fiber suppresses adiposity and the associated parameters of metabolic syndrome. Microbiota-generated fiber-derived short-chain fatty acids (SCFA) and free fatty acid receptors including GPR43 are thought to mediate these effects. We find that while fermentable (inulin), but not insoluble (cellulose) fiber, markedly protected mice against high-fat diet (HFD)-induced metabolic syndrome, the effect was not significantly impaired by either inhibiting SCFA production or genetic ablation of GPR43. Rather, HFD decimates gut microbiota resulting in loss of enterocyte proliferation, leading to microbiota encroachment, low-grade inflammation (LGI) and metabolic syndrome. Enriching HFD with inulin restored microbiota loads, IL-22 production, enterocyte proliferation, and anti-microbial gene expression in a microbiota dependent manner, as assessed by antibiotic and germ-free approaches. Inulin-induced IL-22 expression, which required innate lymphoid cells, prevented microbiota encroachment and protected against LGI and metabolic syndrome. Thus, fermentable fiber protects against metabolic syndrome by nourishing microbiota to restore IL-22-mediated enterocyte function. Dietary fiber supplements suppress adiposity and the associated parameters of metabolic syndrome. Zou et al. show that the fermentable fiber inulin impacts gut microbiota to increase intestinal epithelial proliferation, prevent colonic atrophy, reduce microbiota encroachment into the mucosa, and thereby protect against metabolic syndrome in a microbiota- and IL-22-dependent manner.
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              Transient inability to manage proteobacteria promotes chronic gut inflammation in TLR5-deficient mice.

              Frederic A. Carvalho, Omry Koren, Julia K. Goodrich … (2012)
              Colitis results from breakdown of homeostasis between intestinal microbiota and the mucosal immune system, with both environmental and genetic influencing factors. Flagellin receptor TLR5-deficient mice (T5KO) display elevated intestinal proinflammatory gene expression and colitis with incomplete penetrance, providing a genetically sensitized system to study the contribution of microbiota to driving colitis. Both colitic and noncolitic T5KO exhibited transiently unstable microbiotas, with lasting differences in colitic T5KO, while their noncolitic siblings stabilized their microbiotas to resemble wild-type mice. Transient high levels of proteobacteria, especially enterobacteria species including E. coli, observed in close proximity to the gut epithelium were a striking feature of colitic microbiota. A Crohn's disease-associated E. coli strain induced chronic colitis in T5KO, which persisted well after the exogenously introduced bacterial species had been eliminated. Thus, an innate immune deficiency can result in unstable gut microbiota associated with low-grade inflammation, and harboring proteobacteria can drive and/or instigate chronic colitis. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Gut Microbes
                Journal ID (iso-abbrev): Gut Microbes
                Title: Gut Microbes
                Publisher: Taylor & Francis
                ISSN (Print): 1949-0976
                ISSN (Electronic): 1949-0984
                Publication date (Electronic, pub): 31 January 2020
                Publication date (Electronic, collection): 2020
                Publication date PMC-release: 31 January 2020
                Volume: 11
                Issue: 3
                Pages: 253-264
                Affiliations
                [0001]Institute for Biomedical Sciences, Georgia State University; , Atlanta, GA, USA
                Author notes
                CONTACT Andrew Gewirtz agewirtz@ 123456gsu.edu Institute for Biomedical Sciences, Georgia State University; , Atlanta, GA30303, USA
                Article
                Publisher ID: 1717719
                DOI: 10.1080/19490976.2020.1717719
                PMC ID: 7524291
                PubMed ID: 32005089
                SO-VID: 8574c6e8-c3a0-4b8b-a76c-f4b8a32dd2dd
                Copyright © © 2020 The Author(s). Published with license by Taylor & Francis Group, LLC.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License ( http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

                History
                Page count
                Figures: 1, References: 82, Pages: 12
                Categories
                Subject: Review
                Subject: Review

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: diabetes,inflammation,microbiota metformin,dietary fiber
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: diabetes, inflammation, microbiota metformin, dietary fiber

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