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Gut microbial metabolic signatures in diabetes mellitus and potential preventive and therapeutic applications
- Source :
- Gut Microbes, Vol 16, Iss 1 (2024)
- Publication Year :
- 2024
- Publisher :
- Taylor & Francis Group, 2024.
-
Abstract
- Diabetes mellitus can be subdivided into several categories based on origin and clinical characteristics. The most common forms of diabetes are type 1 (T1D), type 2 diabetes (T2D) and gestational diabetes mellitus (GDM). T1D and T2D are chronic diseases affecting around 537 million adults worldwide and it is projected that these numbers will increase by 12% over the next two decades, while GDM affects up to 30% of women during pregnancy, depending on diagnosis methods. These forms of diabetes have varied origins: T1D is an autoimmune disease, while T2D is commonly associated with, but not limited to, certain lifestyle patterns and GDM can result of a combination of genetic predisposition and pregnancy factors. Despite some pathogenic differences among these forms of diabetes, there are some common markers associated with their development. For instance, gut barrier impairment and inflammation associated with an unbalanced gut microbiota and their metabolites may be common factors in diabetes development and progression. Here, we summarize the microbial signatures that have been linked to diabetes, how they are connected to diet and, ultimately, the impact on metabolite profiles resulting from host-gut microbiota-diet interactions. Additionally, we summarize recent advances relating to promising preventive and therapeutic interventions focusing on the targeted modulation of the gut microbiota to alleviate T1D, T2D and GDM.
Details
- Language :
- English
- ISSN :
- 19490976 and 19490984
- Volume :
- 16
- Issue :
- 1
- Database :
- Directory of Open Access Journals
- Journal :
- Gut Microbes
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.b35676933af4730b110ce696e202552
- Document Type :
- article
- Full Text :
- https://doi.org/10.1080/19490976.2024.2401654