Alterations in intestinal microflora, faecal bile acids and short chain fatty acids in dextran sulphate sodium-induced experimental acute colitis in rats
Y. Araki et al., Alterations in intestinal microflora, faecal bile acids and short chain fatty acids in dextran sulphate sodium-induced experimental acute colitis in rats, EUR J GASTR, 13(2), 2001, pp. 107-112
Background The physiological effects on faecal bile acids and short chain f
atty acids (SCFAs) or intestinal microflora in dextran sulphate sodium (DSS
)-induced colitis remain unknown and are an area of interest.
Design Alterations of these parameters in DSS-induced colitis in rats were
evaluated.
Methods Male Sprague-Dawley rats (n = 10) were given a 3% DSS aqueous solut
ion orally for 7 days. The concentrations of bile acids and SCFAs in the fa
eces were measured using gas chromatography and highperformance liquid chro
matography. Intestinal microflora, especially anaerobes, were investigated
by microbiological methods.
Results On day 7, the concentrations of lithocholic acid and alpha -muricho
lic acid were significantly decreased and that of cholic acid was significa
ntly increased. There was a strong correlation between the concentration of
cholic acid and the macroscopic area of damaged tissue in the colon (R = 0
.74, P < 0.05). With respect to SCFAs, DSS administration significantly dec
reased the concentrations of acetic acid and n-butyric acid. There was also
some correlation between the concentration of acetic acid and macroscopic
damaged area in the colon (R = -0.60, P = 0.07). Bacteriological studies re
vealed significantly decreased eubacteria, bifidobacteria and total anaerob
es after the administration of DSS. In contrast, lactobacilli were signific
antly increased.
Conclusions With the progression of DSS-induced colitis, faecal bile acids,
SCFAs and intestinal microflora were altered. It is possible that these al
terations contribute in part to the progression of DSS-induced colitis. Eur
J Gastroenterol Hepatol 13:107-112 (C) 2001 Lippincott Williams & Wilkins.