Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2020 May 3;11(3):253-264.
doi: 10.1080/19490976.2020.1717719. Epub 2020 Jan 31.

Considering gut microbiota in treatment of type 2 diabetes mellitus

Affiliations

Considering gut microbiota in treatment of type 2 diabetes mellitus

Aneseh Adeshirlarijaney et al. Gut Microbes. .

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.

Keywords: Diabetes; dietary fiber; inflammation; microbiota metformin.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
Overview of how a dysbiotic gut microbiota can promote type 2 diabetes (a) and how microbiota-based therapies might treat and/or prevent this disorder (b).

References

    1. Backhed F, Ley RE, Sonnenburg JL, Peterson DA, Gordon JI.. Host-bacterial mutualism in the human intestine. Science. 2005;307(5717):1915–1920. doi:10.1126/science.1104816. - DOI - PubMed
    1. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature. 2006;444(7122):1027–1031. doi:10.1038/nature05414. - DOI - PubMed
    1. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007;56(7):1761–1772. doi:10.2337/db06-1491. - DOI - PubMed
    1. Backhed F, Manchester JK, Semenkovich CF, Gordon JI. Mechanisms underlying the resistance to diet-induced obesity in germ-free mice. Proc Natl Acad Sci USA. 2007;104(3):979–984. doi:10.1073/pnas.0605374104. - DOI - PMC - PubMed
    1. Adeshirlarijaney A, Zou J, Tran H, Chassaing B, Gewirtz AT. Amelioration of metabolic syndrome by metformin associates with reduced indices of low-grade inflammation independently of the gut microbiota. Am J Physiol Endocrinol Metab. 2019. doi:10.1152/ajpendo.00245.2019. - DOI - PMC - PubMed

MeSH terms