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Ann N Y Acad Sci. 2012 Jul;1258:52-9. doi: 10.1111/j.1749-6632.2012.06553.x.

Microbial butyrate and its role for barrier function in the gastrointestinal tract.

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1
Institute of Veterinary Physiology, Free University of Berlin, Berlin, Germany.

Abstract

Butyrate production in the large intestine and ruminant forestomach depends on bacterial butyryl-CoA/acetate-CoA transferase activity and is highest when fermentable fiber and nonstructural carbohydrates are balanced. Gastrointestinal epithelia seem to use butyrate and butyrate-induced endocrine signals to adapt proliferation, apoptosis, and differentiation to the growth of the bacterial community. Butyrate has a potential clinical application in the treatment of inflammatory bowel disease (IBD; ulcerative colitis). Via inhibited release of tumor necrosis factor α and interleukin 13 and inhibition of histone deacetylase, butyrate may contribute to the restoration of the tight junction barrier in IBD by affecting the expression of claudin-2, occludin, cingulin, and zonula occludens poteins (ZO-1, ZO-2). Further evaluation of the molecular events that link butyrate to an improved tight junction structure will allow for the elucidation of the cofactors affecting the reliability of butyrate as a clinical treatment tool.

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