Microbial butyrate and its role for barrier function in the gastrointestinal tract.
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.
Institute of Veterinary Physiology, Free University of Berlin, Berlin, Germany.
Svenja
S
Plöger
Friederike
F
Stumpff
Gregory B
GB
Penner
Jörg-Dieter
JD
Schulzke
Gotthold
G
Gäbel
Holger
H
Martens
Zanming
Z
Shen
Dorothee
D
Günzel
Joerg R
JR
Aschenbach
D001419:Bacteria / Q000378:metabolism*; D020148:Butyric Acid / Q000378:metabolism*; D005285:Fermentation; D005753:Gastric Mucosa / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism / Q000502:physiology*; D019108:Tight Junctions / Q000502:physiology
D020148:Butyric Acid