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Butyrate transport deficiency in patients with inflammatory bowel disease: Clinical and pathophysiological implications

Authors
  • Thibault, Ronan
  • Segain, Jean-Pierre
Publication Date
Jan 01, 2011
Identifiers
DOI: 10.1016/j.nupar.2011.04.002
OAI: oai:HAL:hal-02642347v1
Source
HAL-Descartes
Keywords
Language
French
License
Unknown
External links

Abstract

In the early 1980s, ulcerative colitis (UC) was considered to be a consequence of butyrate oxidation deficiency in the colonic mucosa, and so, a metabolic disease. The short-chain fatty acid butyrate, which is mainly produced in the lumen of the large intestine by the fermentation of dietary fibers, is the preferred energy source for the colonocyte and plays a major role in the physiology of the colonic mucosa. Recent data indicate that the butyrate oxidation deficiency is a consequence of its reduced intracellular availability, due to the inflammation-related down-regulation of the monocarboxylate transporter MCTI. MCTI expression levels, so butyrate oxidation, are inversely correlated to the intensity of inflammation. The loss of MCTI expression could explain the lack of efficacy of butyrate enemas in severe UC. This could also lead to the inhibition of butyrate regulatory effects on cell proliferation / apoptosis balance and favour inflammatory bowel diseases-associated colorectal carcinogenesis. (C) 2011 Elsevier Masson SAS. All rights reserved.

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