An investigation was carried out to determine whether variations of dietary carbohydrates could modify the colonic flora in rats. Sprague‐Dawley rats were fed with two equicaloric diets based on the AIN‐76 diet ( American Institute of Nutrition 1977) but differing from that diet in content of carbohydrates, i.e. high sucrose (64%) or high corn starch (64%). Feeding was continued for 9 months ad libitum and no variation in weight gain was recorded among the different diets. A prevalence of aerobes, and a significant reduction in the ratio anaerobes/aerobes in the faeces of rats on the high starch diet compared with the high sucrose diet, was observed. The anaerobe genera identified included Actinomyces, Bacteroides, Bifidobacterium, Clostridium, Eubacterium, Lactobacillus and Propionibacterium. Bacteroides was the most prevalent genus in both dietary groups (51·2 and 29·5% in the faeces of rats fed the sucrose and starch diets, respectively). In contrast, clostridia were prevalent in the starch‐fed group (23·8%) and less so in the sucrose diet (11·5%), as propionibacteria were prevalent in faeces of rats fed the starch diet (15·5%), and low in the sucrose diet (3·9%). The remaining genera were scarce in faeces from rats on either diet. Total short‐chain fatty acids (SCFA) were significantly higher in the faeces of animals fed the starch diet compared with those fed the sucrose diet. The relative concentrations of acetic, propionic and butyric acids were not significantly different between the two dietary groups. In conclusion, high starch diet can markedly modify the composition of faecal flora and alter considerably the faecal concentration of SCFAs, compounds which might have a health‐promoting effect.

No abstract

Apoptosis of tumor cells is an important growth-regulating event in tumor masses. In this study we have confirmed that deoxycholic acid (DCA) and the short-chain fatty acids (SCFA) butyrate and propionate induce a time- and concentration-dependent apoptosis in two human colon tumor cell lines: HT-29 and CaCO2. DCA is more potent, inducing effects at low concentration (50 microM) and after 24 hours of incubation, whereas SCFA (4 mM) requires 72-96 hours of treatment. Combining low concentrations of DCA (12.5-25 microM) with butyrate and propionate (4 mM) produces an additive effect on the percentage of apoptotic cells, as demonstrated by flow cytometry and DNA fragmentation. Protein kinase C, protein tyrosine kinase, and gene transcription/translation inhibitors do not significantly modify the rate of apoptosis, whereas the intracellular Ca2+ chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester (BAPTA-AM) completely abolishes the DCA-induced effect without affecting the SCFA-induced apoptosis. Measurement of intracellular Ca2+ by inverted fluorescence microscopy reveals that DCA induces a rapid increase of cytosolic Ca2+ that is abolished when the cells are preincubated with BAPTA-AM, whereas ethyleneglycolbis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid has a minimal effect. In contrast, SCFA does not modify the intracellular Ca2+ concentration. Thus the DCA-induced apoptosis is a Ca(2+)-dependent process, whereas the intracellular signals responsible for the SCFA-induced effect remain unknown. The ionophore activity of DCA could be responsible for the increased intracellular Ca2+, but other mechanisms, such as activation of phospholipase C and phosphoinositide hydrolysis, have to be considered.

No abstract

We studied the effects of sucrose or starch in the diet (460 g/kg diet) on fecal bile acid concentrations in Sprague Dawley rats after 4 wk of feeding. Total bile acid concentration in the feces was significantly lower in the rats fed the starch diet than in those fed the sucrose diet (4.56 +/- 0.47 mg/g dry weight and 8.03 +/- 0.94, respectively, SEM), due to a reduction of deoxycholic, alpha-muricholic and beta-muricholic acids. Fecal and cecal pH values were significantly lower in the rats fed the starch diet compared to those fed the sucrose diet (6.79 +/- 0.08 and 7.15 +/- 0.09 for fecal pH and 7.02 +/- 0.05 and 7.2 +/- 0.04 for cecal pH in the two diet groups, respectively). Colon proliferation was also significantly lower in the starch-fed rats compared to those fed sucrose (labeling index 3.51 +/- 0.6 and 5.69 +/- 0.74, respectively), and the reduction was apparent in the middle and upper compartments of the colon crypts. The mucosal proliferation, expressed as percentage of labeled cells in the upper compartment of the colon crypts, was positively correlated with the concentration of deoxycholic, lithocholic, alpha-muricholic, beta-muricholic, cholic and total bile acids in the feces (per gram wet weight). The results indicate a protective effect of starch versus sucrose diets on colon mucosa.