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Gut 2000;46:447-448; doi:10.1136/gut.46.4.447
Copyright © 2000 BMJ Publishing Group Ltd & British Society of Gastroenterology.
Gut 2000;46:447-448 ( April )

Commentary

See articles on pages 493 and 507

The intracellular target of butyrate's actions: HDAC or HDON'T?

The first 150 words of the full text of this article appear below.

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 beta -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 . . . [Full text of this article]


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