The
short-chain fatty acid butyrate, which is mainly produced in the lumen of the large intestine by the fermentation of
dietary fibers, plays a major role in the physiology of the colonic mucosa. It is also the major energy source for the colonocyte. Numerous studies have reported that
butyrate metabolism is impaired in intestinal inflamed mucosa of patients with
inflammatory bowel disease (IBD). The data of
butyrate oxidation in normal and inflamed colonic tissues depend on several factors, such as the methodology or the models used or the intensity of
inflammation. The putative mechanisms involved in
butyrate oxidation impairment may include a defect in beta oxidation,
luminal compounds interfering with
butyrate metabolism, changes in
luminal butyrate concentrations or pH, and a defect in
butyrate transport. Recent data show that
butyrate deficiency results from the reduction of
butyrate uptake by the inflamed mucosa through downregulation of the monocarboxylate transporter MCT1. The concomitant induction of the
glucose transporter GLUT1 suggests that
inflammation could induce a metabolic switch from
butyrate to
glucose oxidation.
Butyrate transport deficiency is expected to have clinical consequences. Particularly, the reduction of the intracellular availability of
butyrate in colonocytes may decrease its protective effects toward
cancer in IBD patients.