Déficit de transport du butyrate chez les patients atteints de maladies inflammatoires chroniques de l’intestin : implications cliniques et physiopathologiques

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 MCT1. MCT1 expression levels, so butyrate oxidation, are inversely correlated to the intensity of inflammation. The loss of MCT1 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.