This describes the biochemical action where the short-chain fatty acid butyrate blocks the enzymatic activity of histone deacetylases (HDACs). This inhibition is a critical epigenetic mechanism that alters chromatin structure, leading to increased gene transcription. Clinically, this process is significant for modulating gene expression related to cellular differentiation, apoptosis, and immune regulation, particularly within the gastrointestinal tract.
Origin
The term draws from “butyrate,” a fermentation product of dietary fiber by the gut microbiota, and the established molecular process of “histone deacetylase inhibition.” Histone modification and the role of HDACs in gene regulation were elucidated in molecular biology, with butyrate later identified as a potent, naturally occurring inhibitor. This convergence highlights the direct influence of the gut microbiome on host epigenetics and systemic health.
Mechanism
Butyrate acts by directly binding to the active site of HDAC enzymes, preventing them from removing acetyl groups from histone proteins. The resulting hyperacetylation of histones loosens the chromatin structure, making specific gene promoters more accessible to transcription factors. This mechanism promotes the expression of beneficial genes, including those involved in gut barrier function, anti-inflammatory pathways, and potentially the regulation of metabolic hormones.
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