A colorimetric method was used on water-soluble much extracted from m u d scraping!? and contents of the caecum and the colon of five germ-free (GF) rats and five heteroxenic (HE) rats harbouring a hnmao flora (GF rats d a t e d with a human flora). These rats were fed on a diet containing either 100 g sucrose/kg or 100 g inulin/kg. Histological stains, periodic aciMChiff, alcian blue pH 2.5 and alcian blue pH0-5 were used to discriminate between neutral, acidic and acidic sulphated mucins respectively. Spectrocolorimetric assays led to a calculated absorbance value for 1 mg of the initial much extract. Each much type was compared between treatments. The caecal contents of GF rats contained more acidic mucin than sulphomucin, which was present in the same proportion as neutral mucin. Their colonic contents contained more acidic mucins than sulphomucin, which in turn was more abundant than neutral mucin. Their caecal mucosa mucin distribution differed from that of the contents: very little acidic much was present and neutral and dphomucin proportions were of the same order of magnitude. Inulin increased the amount of neutral much in the caecal contents and of sulphated mucios in the colonic contents and increased the amounts of neutral and acidic mucins in the caecal mucwa. Mucin distribution in the HE rats was very different from that in the GF rats: the caecal contents contained a high proportion of acidic m u c h and very little sulphomucin. The same distribution of mucins was observed in the colonic contents. The caecal mucaw contained less acidic much and more sulphomucin than the caecal contents. Inulin decreased acidic mucins and increased sulphated m u c h in the caecal contents and increased neutral and sulphated mucins in the colonic contents. Inulin increased sulphomucin in the caecal m u m and decreased acidic much in the caecal and colonic mucosas. The very low amount of mucin that was recovered in the colonic mucosa suggests that, in the presence of the bacterial flora and associated with inulin in the diet, much was extensively released from the mucosa to the colonic lumen. This might be related to the bacterial metabolites produced.

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The present study examined whether the intestinal microflora could affect the bioavailability and vitamin A activity of dietary aand b-carotene in the rat. In the first set of experiments, we used conventional, germ-free (axenic), and human-flora-associated (heteroxenic) rats. In a second series, conventional rats were treated with either an antibiotic mixture or a potent inhibitor of gastric secretion (Omeprazole). All animals were first depleted of vitamin A over 4 weeks and then were fed on a sterilized diet supplemented with 14 mg b-carotene and 3 mg a-carotene/kg for 2 weeks. In both experiments, a reduction in the intestinal microflora resulted in an increased storage of b-carotene, a-carotene and vitamin A in the liver. Neither the nature of the metabolism of the intestinal microflora (aerobic or anaerobic) nor treatment with omeprazole, to modify intestinal pH, induced a significant effect on the measured variables. When incubated with 15 mol b-carotene/l for 72 h, neither the anaerobic nor the aerobic sub-fractions obtained from rat or human faeces contributed to b-carotene degradation or to vitamin A synthesis. These findings suggest that reduction in gut microflora results in a better utilization of aand b-carotene by rats, although bacteria do not have a direct effect on the bioavailability of these pigments.

One of the most recent hypotheses concerning the protective effect of some dietary ®bres against colon cancer implicates butyrate. Very few publications have addressed its possible in¯uence on the phase II enzymes and on the bacterial enzymes involved in the enterohepatic recirculation of toxic compounds. We used an original model of monoxenic rats oriented towards the preferential production of butyrate. Fischer male germ-free rats were mono-associated with a strain of Clostridium paraputri®cum. They were fed either a control diet or a lactulose-enriched diet for 6 weeks. In the caeco-colon the speci®c activities (SAs) of the microsomal enzymes (glutathione-Stransferase and UDP-glucuronosyl-transferase) were 1.7-fold those of the control rats. In the intestine and liver the SAs of the phase II enzymes were not altered, nor was the hepatic cytochrome P450. In the caecum of the lactulose-fed rats the SA of b-glucuronidase decreased by 27% and that of b-glucosidase doubled. The chronic consumption of lactulose doubled the total caecal short-chain fatty acids, and the production of butyrate was enhanced. Since the germ-free rats behaved differently when fed the same diets, we concluded that the fermentation products of lactulose (and not the lactulose itself) were involved in the effects we describe. The involvement of butyrate in this phenomenon is discussed.

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