ArticleFrontiers in endocrinology2025
Inulin and
Article in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Molecular mechanisms and structure-activity relationships of natural polysaccharides in ameliorating type 2 diabetes mellitus: a comprehensive review.Frontiers in nutrition · 2026Review
- Natural polysaccharides as immunometabolic modulators in metabolic diseases: mechanisms and translational challenges.Frontiers in immunology · 2026Review
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Authors and funding
10 authors.
Funding
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Abstract
Background: Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease that poses a serious threat to health. Currently, there are no completely effective treatment options. Modulating intestinal flora and its metabolites may represent a promising new approach for diabetes therapy. Regulating intestinal microbiota and its metabolites through prebiotics, mediated by regulatory T (Treg) cells, could offer a novel strategy to improve the chronic inflammatory state associated with diabetes. Objective: This study aimed to investigate the improvement of diabetes-related chronic inflammation by examining the effects of inulin (INU) and Methods: A diabetic rat model was established using a high-fat diet and streptozotocin (STZ) injection. Sprague-Dawley rats were randomly allocated into four groups: type 2 diabetes mellitus (T2DM), T2DM with INU group (T2DM + INU), T2DM with LBP group (T2DM + LBP), and T2DM with INU and LBP group (T2DM + INU + LBP). After 8 weeks of intervention, the rats were euthanized, and relevant pathophysiological and biochemical indicators were analyzed. Results: INU and LBP treatments significantly decreased the levels of inflammatory cytokines, including MCP-1, IL-18, NF-κB, NLRP3, superoxide dismutase (SOD), and malondialdehyde (MDA). Moreover, these alleviations of the inflammatory state of diabetes were partially attributed to the increased proportion of Treg cells. We found that the abundance of tauro β-muricholic acid (TβMCA) was reduced following INU and LBP treatment, whereas the relative abundances of chenodeoxycholic acid (CDCA), lithocholic acid (LCA), and hyocholic acid (HCA) were all increased compared to those in the untreated group. Mechanically, INU and LBP significantly influenced the negative feedback regulation of the FXR-FGF15-FGFR4 axis via intestinal bile acids, thereby increasing the proportion of Treg cells in the periphery of diabetic rats. Intriguingly, an increase in Treg cells after INU and LBP intervention was notably correlated with the improvement in the inflammatory state of diabetes. Conclusions: INU and LBP modulate bile acids derived from intestinal flora to improve the chronic inflammatory status of diabetic rats. Specifically, both exert their effectiveness by regulating gut microbial bile acid metabolites through the FXR-FGF15-FGFR4 axis to activate Treg cells. These findings provide an experimental basis for further exploration of the mechanism underlying the effects of this combination in diabetic animal models, which may contribute to clinical therapeutic practice for the control of the disease.
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