Article3 Biotech2026
Study on the role and clinical relevance of gut microbiota in diabetic foot ulcers.
Article in 3 Biotech, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
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Abstract
Diabetic foot ulcers (DFU) are severe and costly complications of diabetes, predisposing to infection, amputation, and mortality, highlighting the urgent need to clarify their mechanisms for optimized clinical management. This study integrated clinical biochemistry data and multi-omics analyses (including metagenomic sequencing) from 11 patients to reveal the critical role of gut microbiota in the pathogenesis of DFU. Results showed significant host metabolic disorders in DFU patients, characterized by hypoalbuminemia (mean ± SD:32.35 ± 6.02 g/L), persistent hyperglycemia (mean ± SD:8.25 ± 3.21 mmol/L), and imbalances in trace elements such as magnesium (mean ± SD:0.84 ± 0.08 mmol/L). Concurrently, the gut microbiota composition was markedly altered, with enrichment of the phylum Bacillota_A (formerly Firmicutes; 48.7% in patients vs. 32.1% in controls) and elevated genetic potential of virulence genes (e.g., type VI secretion systems, capsular polysaccharide gene cps4J/L). Metagenomic tracing revealed that antibiotic resistance genes (ARGs) such as tet(A) and blaOXA-1 were co-localized with mobile genetic elements (MGEs) including IncF plasmids and tnpA transposases. 99.2% of key ARGs shared sequence homology with gut-derived metagenome-assembled genomes (MAGs) and co-localized with MGEs, indicating potential cross-niche transfer capacity. Furthermore, renal (mean ± SD:11.81 ± 5.75 mmol/L) and hepatic (ALT: 35.67 ± 18.22 U/L) dysfunction correlated with aggravated gut dysbiosis and ARG enrichment. In conclusion, this study confirms that host metabolic deficiencies contribute to DFU refractoriness by altering gut microbiota ecology and enhancing horizontal gene transfer of virulence and resistance determinants, providing a novel framework for precision therapies targeting the host-microbe metabolic interface. Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-026-04745-8.
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