ReviewFrontiers in microbiology2026
Epigenetics, bacterial metabolites and type 2 diabetes: a new view of gut-genome interactions.
Review in Frontiers in microbiology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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8 authors.
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Abstract
Type 2 diabetes (T2D) is traditionally viewed as a disorder of glucose homeostasis, yet growing evidence suggests that its pathogenesis is deeply influenced by interactions between the gut microbiota and host gene regulation. Bacterial metabolites have emerged as key molecular mediators capable of linking environmental exposures, metabolism and epigenetic control of gene expression. These insights are reshaping current understanding of how microbial signals contribute to metabolic disease. This review examines the emerging role of bacterial metabolites as modulators of host epigenetic landscapes in T2D. We discuss how short-chain fatty acids (SCFAs), particularly butyrate and propionate, regulate chromatin accessibility through histone deacetylase inhibition and changes in histone acetylation. Beyond SCFAs, we highlight additional classes of microbiota-derived metabolites, including tryptophan-derived indoles such as indole-3-propionic acid, polyamines such as spermidine and aromatic amino acid derivatives, that expand the microbiota-epigenetic axis through mechanisms involving DNA methylation, transcriptional regulation, mitochondrial function and inflammatory signaling. These effects occur in a tissue-specific manner across metabolically relevant organs including the colon, liver, pancreatic
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