4.6 Article

Abnormal gut microbiota composition contributes to the development of type 2 diabetes mellitus in db/db mice

Journal

AGING-US
Volume 11, Issue 22, Pages 10454-10467

Publisher

IMPACT JOURNALS LLC
DOI: 10.18632/aging.102469

Keywords

gut microbiota; diabetes mellitus; pseudo-germ-free mice

Funding

  1. National Natural Science Foundation of China [81771159, 81571047, 81703482, 81974171]
  2. Program of Bureau of Science and Technology Foundation of Changzhou [CJ20159022, CJ20160030]
  3. Major Science and Technology Projects of Changzhou Municipal Committee of Health and Family Planning [ZD201505, ZD201407]
  4. Changzhou High-Level Medical Talents Training Project [2016ZCL J020]

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It is well recognized that type 2 diabetes mellitus (T2DM) is an age-related metabolic disease, emerging gradually as a major global health burden that has gained public attention. Meanwhile, increasing attention is paid to the crucial role of gut microbiota in the pathogenesis and therapeutic mechanisms of metabolic disorders, especially T2DM. In this study, we used C57 BL/KS db/db male mice as a T2DM murine model. We found that the beta-diversity and relative abundances of gut bacteria were obviously altered in db/db mice, associated with a significant increase in Verrucomicrobia at six levels (phylum, class, order, etc.) and family S24-7 and a significant decrease in Bacteroidaceae at family, genus, and species levels, as well as Prevotellaceae at family and genus levels. Furthermore, fecal bacteria from db/db and m/m mice transplanted into pseudo-germ-free mice showed a significant change in the metabolic parameters, including the body weight, fasting blood glucose, fluid and food intake, and alterations in the composition of the gut microbiota. Taken together, these findings suggest that abnormalities in the composition of the gut microbiota might contribute to the development of T2DM and that potential therapeutic strategies improving gut microbiota might provide beneficial effects for individuals with T2DM and age-related glucose intolerance.

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