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Editorial
. 2025 Jan 15;16(1):100376.
doi: 10.4239/wjd.v16.i1.100376.

Influence of gut bacteria on type 2 diabetes: Mechanisms and therapeutic strategy

Affiliations
Editorial

Influence of gut bacteria on type 2 diabetes: Mechanisms and therapeutic strategy

Xue Wen et al. World J Diabetes. .

Abstract

The onset and progression of type 2 diabetes mellitus (T2DM) are strongly associated with imbalances in gut bacteria, making the gut microbiome a new potential therapeutic focus. This commentary examines the recent publication in World Journal of Diabetes. The article explores the association between T2DM and gut microbiota, with a focus on the pathophysiological changes related to dysbiosis. It proposes innovative microbiome-targeted therapeutic strategies and evaluates the challenges and future directions of such approaches. This editorial summarizes the key points of their discussion of the role of the gut microbiome in T2DM and elaborates on the influence of specific gut microbial species on the disease through the host-microbiota metabolic axis. It provides new insights for future research on gut-microbiota-based interventions for T2DM.

Keywords: Biological pathways; Intestinal axis; Intestinal microbiome; Short-chain fatty acids; Treatment; Type 2 diabetes.

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Conflict of interest statement

Conflict-of-interest statement: All other authors declare no competing interests.

Figures

Figure 1
Figure 1
Intestinal bacteria and type 2 diabetes mellitus. TM2D: Type 2 diabetes mellitus.
Figure 2
Figure 2
Mechanisms of action of specific gut microbiota affecting various organs. The left side illustrates the mechanisms by which beneficial bacteria, such as Bifidobacterium, affect the skin, kidneys, and brain, while the right side shows the impact of harmful bacteria like Fusobacterium on these organs. CYSC: Cystatin; EGFR: Estimated glomerular filtration rate; GLP-1: Glucagon-like peptide-1; IL: Interleukin; LPS: Lipopolysaccharide; PRO: Protein; PCS: Phosphatidylcholines; SCr: Sex combs reduced; SCFAs: Short-chain fatty acids; TGF-β1: Transforming growth factor β1; TNFR1: Tumor necrosis factor receptor 1.

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