%0 Journal Article
%T The epigenetic effects of butyrate: potential therapeutic implications for clinical practice
%A Roberto Berni Canani
%A Margherita Di Costanzo
%A Ludovica Leone
%J Clinical Epigenetics
%D 2012
%I BioMed Central
%R 10.1186/1868-7083-4-4
%X The intestinal microbiota plays a critical role in the establishment and maintenance of body health. Commensal bacteria are involved in the fermentation of dietary fibers in the colon leading to production of short chain fatty acids (SCFAs), 2-carbon to 5-carbon weak acids including acetate (C2), propionate (C3), butyrate (C4) and valerate (C5). Among the SCFAs, butyrate has received particular attention for its multiple beneficial effects from the intestinal tract to the peripheral tissues [1]. The most important butyrate producers appear to be Faecalibacterium prausnitzii, which belongs to the Clostridium leptum (or clostridial cluster IV) cluster, and Eubacterium rectale/Roseburia spp., which belong to the Clostridium coccoides (or clostridial cluster XIVa) cluster of firmicute bacteria [2]. The mechanisms of action of butyrate are multiple, but many of these are related to its regulatory effects on gene expression. Butyrate is part of a well known class of epigenetic substances known as histone deacetylase inhibitors (HDACi). Epigenetics focuses on the mechanisms that mold chromatin structures and regulate gene expression with stability, thus defining cell identity and function and adapting cells to environment, without changing the nucleotide sequence. There are three distinct, but closely interacting, epigenetic mechanisms (histone acetylation, DNA methylation, and non-coding microRNAs) that are responsible for modifying the expression of critical genes associated with physiologic and pathologic processes [3]. Histone tail acetylation is believed to enhance the accessibility of a gene to the transcription machinery, whereas deacetylated tails are highly charged and believed to be tightly associated with the DNA backbone, thus limiting accessibility of genes to transcription factors [4]. Modulation of histone acetylation and deacetylation through environmental factors, including dietary compounds, may prevent diseases and maintain health. In a broader context,
%K epigenome
%K histone deacetylase inhibitor
%K short chain fatty acids
%U http://www.clinicalepigeneticsjournal.com/content/4/1/4