ArticleFrontiers in endocrinology2026
Dietary butyrate alleviates high-fat diet-induced colonic mucosal impairment accompanied by increased gut-derived indole-3-acetic acid and enhanced PPARγ signaling.
Article in Frontiers in endocrinology, 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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Abstract
Introduction: High-fat diet (HFD) induces intestinal barrier impairment, associated with gut microbiota dysbiosis, endotoxin translocation and metabolic dysfunction. Dietary butyrate has been reported to improve intestinal homeostasis, but the underlying mechanism remains incompletely understood. This study aimed to investigate the effects of dietary butyrate on HFD-induced colonic mucosal dysfunction and to explore underlying mechanisms with respect to the role of gut microbiota and its metabolites. Methods: Male APOE*3-Leiden.CETP mice, a well-established translational model for diet-induced metabolic dysfunction, were fed an HFD with or without 5% sodium butyrate. Metabolic phenotypes, plasma lipopolysaccharide (LPS), colonic histology, inflammatory responses, and tight junction-associated changes were assessed. Fecal microbiota transplantation (FMT) was performed in antibiotic-treated recipient mice to assess the contribution and transferability of butyrate-shaped gut microbiota. Cecal metagenomic sequencing and LC/MS-based colonic indole-3-acetic acid (IAA) measurement were performed. Caco-2 cells were used to assess the direct effects of sodium butyrate and IAA on enterocytes and to determine, through pioglitazone treatment and PPARγ knockdown, whether PPARγ mediates IAA-induced enterocyte responses. Results: Dietary butyrate induced favorable changes in multiple colonic barrier-associated parameters, including improved colonic architecture, lower circulating LPS levels, decreased Conclusion: Dietary butyrate improves colonic mucosal homeostasis under HFD feeding, accompanied by gut microbial remodeling and increased colonic IAA levels. Together with the PPARγ-dependent epithelial response to IAA observed in Caco-2 cells, these findings suggest a potential mechanistic framework linking butyrate-associated microbial changes, IAA metabolism, and epithelial PPARγ signaling.
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