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    Microbial butyrate and its role for barrier function in the gastrointestinal tract (2012)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Plöger, S (WE 2)
    Stumpff, Friederike (WE 2)
    Penner, G. B.
    Schulzke, J. D.
    Gäbel, G.
    Martens, H (WE 2)
    Shen, Z.
    Günzel, D.
    Aschenbach, Jörg R. (WE 2)
    Quelle
    Annals of the New York Academy of Sciences; 1258 — S. 52–59
    ISSN: 0077-8923
    Sprache
    Englisch
    Verweise
    DOI: 10.1111/j.1749-6632.2012.06553.x.
    Pubmed: 22731715
    Kontakt
    Institut für Veterinär-Physiologie

    Oertzenweg 19 b
    14163 Berlin
    +49 30 838 62600
    physiologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    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.