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The intracellular target of butyrate's actions: HDAC or HDON'T?
  1. University of Melbourne Department of Medicine
  2. The Royal Melbourne Hospital
  3. Victoria, 3050 Australia

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    Butyrate, the four-carbon short chain fatty acid, has special significance for clinicians and scientists interested in large bowel physiology. It is normally present in the colonic lumen at millimolar concentrations as a product of bacterial fermentation of luminal carbohydrates and is readily taken up by the colonic epithelium to be used as a major energy source via β-oxidation. Butyrate affects key functions of the colonic epithelium in vivo or at least in vitro in models of the colonic epithelium. These functions include promotion of sodium and water absorption, improvement of tight junction permeability, and acceleration of epithelial restitution. Thus, butyrate plays an important role in the maintenance of colonic mucosal health.

    Butyrate has also been implicated in the pathogenesis of colonic diseases, especially colorectal cancer and ulcerative colitis. Butyrate's role in the pathogenesis of ulcerative colitis has been a fascinating saga. In 1981, Roediger first reported that epithelial cells isolated from the rectum of patients with ulcerative colitis exhibited impaired β-oxidation of butyrate.1 His “energy-deficiency” hypothesis created more attention when diversion colitis, which may histologically resemble ulcerative colitis, was shown to be largely caused by a deficient supply of short chain fatty acids in the lumen.2 Whether a defect in β-oxidation has specificity for ulcerative colitis and indeed whether it …

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