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

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

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bacteria / metabolism*
  • Butyric Acid / metabolism*
  • Fermentation
  • Gastric Mucosa / metabolism
  • Gastric Mucosa / physiology*
  • Humans
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / physiology*
  • Tight Junctions / physiology

Substances

  • Butyric Acid