Ability of Lactobacillus fermentum to overcome host α-galactosidase deficiency, as evidenced by reduction of hydrogen excretion in rats consuming soya α-galacto-oligosaccharides

<p>Abstract</p> <p>Background</p> <p>Soya and its derivatives represent nutritionally high quality food products whose major drawback is their high content of α-galacto-oligosaccharides. These are not digested in the small intestine due to the natural absence of tissular α-galactosidase in mammals. The passage of these carbohydrates to the large intestine makes them available for fermentation by gas-producing bacteria leading to intestinal flatulence. The aim of the work reported here was to assess the ability of α-galactosidase-producing lactobacilli to improve the digestibility of α-galacto-oligosaccharides <it>in situ</it>.</p> <p>Results</p> <p>Gnotobiotic rats were orally fed with soy milk and placed in respiratory chambers designed to monitor fermentative gas excretion. The validity of the animal model was first checked using gnotobiotic rats monoassociated with a <it>Clostridium butyricum </it>hydrogen (H₂)-producing strain. Ingestion of native soy milk by these rats caused significant H₂emission while ingestion of α-galacto-oligosaccharide-free soy milk did not, thus validating the experimental system. When native soy milk was fermented using the α-galactosidase-producing <it>Lactobacillus fermentum </it>CRL722 strain, the resulting product failed to induce H₂emission in rats thus validating the bacterial model. When <it>L. fermentum </it>CRL722 was coadministered with native soy milk, a significant reduction (50 %, <it>P </it>= 0.019) in H₂emission was observed, showing that α-galactosidase from <it>L. fermentum </it>CRL722 remained active <it>in situ</it>, in the gastrointestinal tract of rats monoassociated with <it>C. butyricum</it>. In human-microbiota associated rats, <it>L. fermentum </it>CRL722 also induced a significant reduction of H₂emission (70 %, <it>P </it>= 0.004).</p> <p>Conclusion</p> <p>These results strongly suggest that <it>L. fermentum </it>α-galactosidase is able to partially alleviate α-galactosidase deficiency in rats. This offers interesting perspectives in various applications in which lactic acid bacteria could be used as a vector for delivery of digestive enzymes in man and animals.</p

Production of volatile fatty acids as a result of bacterial interactions in the cecum of gnotobiotic rats and chickens fed a lactose-containing diet.

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Increased induction of apoptosis by Propionibacterium freudenreichii TL133 in colonic mucosal crypts of human microbiota-associated rats treated with 1,2-dimethylhydrazine

Propionibacterium freudenreichii, a food-grade bacterium able to kill colon cancer cell lines in vitro by apoptosis, may exert an anticarcinogenic effect in vivo. To assess this hypothesis, we administered daily 2 £ 1010 colony-forming units (CFU) of P. freudenreichii TL133 to human microbiota- associated (HMA) rats for 18 d. Either saline or 1,2-dimethylhydrazine (DMH) was also administered on days 13 and 17 and rats were killed on day 19. The levels of apoptosis and proliferation in the mid and distal colon were assessed by terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate nick end labelling (TUNEL) and proliferating cell nuclear antigen (PCNA) immunolabelling, respectively. The administration of P. freudenreichii TL133 significantly increased the number of apoptotic cells in DMH-treated rats compared to those given DMH only (P,0·01). Furthermore, propionibacteria were able to decrease the proliferation index in the distal colon after treatment with DMH (P,0·01). Conversely, propionibacteria alone did not exert such an effect on healthy colonic mucosa. P. freudenreichii TL133 thus facilitated the elimination of damaged cells by apoptosis in the rat colon after genotoxic insult and may play a protective role against colon cancer

Protective effects of Brussels sprouts, oligosaccharides and fermented milk towards 2-amino-3-methylimidazo[4,5-f]quinoline (IQ)-induced genotoxicity in the human flora associated F344 rat: role of xenobiotic metabolising enzymes and intestinal microflora

International audienceWe investigated the chemoprotective effects of four common constituents of the human diet, i.e. a fermented milk, inulin, oligofructose and Brussels sprouts, towards 2-amino-3-methylimidazo[4,5-f]quinoline (IQ)-induced genotoxicity in male Fischer 344 rats harbouring a human intestinal microflora. We found that the four dietary components significantly reduced IQ-induced DNA damage in hepatocytes (reduction ranged from 74% with inulin to 39% with Brussels sprouts) and colonocytes (reduction ranged from 68% with inulin to 56% with Brussels sprouts). This chemoprotective effect correlated with the induction of hepatic UDP-glucuronosyl transferase following Brussels sprouts consumption, and with alterations of bacterial metabolism in the distal gut (acidification, increase of butyrate proportion, decrease of β-glucuronidase activity) following inulin consumption

Apple proanthocyanidins do not reduce the induction of preneoplastic lesions in the colon of rats associated with human microbiota

Since the gut microbiota metabolizes various dietary constituents unabsorbed by the small intestine and modulates colon function, it plays an essential role in colon carcinogenesis. First, we have developed a model of human microbiota-associated rats (HMA), fed a human-type diet and injected with 1-2,dimethylhydrazine (DMH). We observed that the number and size of DMH-induced aberrant crypt foci (ACF) were significantly higher in HMA rats than in germ-free or conventional rats. Second, we used this model to assess the protective effect of an apple proanthocyanidin-rich extract (APE) on colon carcinogenesis. In this model, ACF number and multiplicity were not reduced by APE at 0.001% and 0.01% in drinking water. They were higher with APE 0.1% than with APE 0.01%. Therefore, the cross-talk between human microbiota and the colon epithelium should be taken into account in carcinogenesis models. Moreover, attention should be paid prior to using proanthocyanidin extracts as dietary supplements for humans

Gut microbiota richness promotes its stability upon increased dietary fibre intake in healthy adults.

Gut microbiota richness and stability are important parameters in host-microbe symbiosis. Diet modification, notably using dietary fibres, might be a way to restore a high richness and stability in the gut microbiota. In this work, during a 6-week nutritional trial, 19 healthy adults consumed a basal diet supplemented with 10 or 40 g dietary fibre per day for 5 days, followed by 15-day washout periods. Fecal samples were analysed by a combination of 16S rRNA gene pyrosequencing, intestinal cell genotoxicity assay, metatranscriptomics sequencing approach and short-chain fatty analysis. This short-term change in the dietary fibre level did not have the same impact for all individuals but remained significant within each individual gut microbiota at genus level. Higher microbiota richness was associated with higher microbiota stability upon increased dietary fibre intake. Increasing fibre modulated the expression of numerous microbiota metabolic pathways such as glycan metabolism, with genes encoding carbohydrate-active enzymes active on fibre or host glycans. High microbial richness was also associated with high proportions of Prevotella and Coprococcus species and high levels of caproate and valerate. This study provides new insights on the role of gut microbial richness in healthy adults upon dietary changes and host microbes' interaction

Ability of to overcome host α-galactosidase deficiency, as evidenced by reduction of hydrogen excretion in rats consuming soya α-galacto-oligosaccharides-4

Hambers were analyzed for Hconcentration using GC. Treatments successively applied to all rats (for more details, see Material and Methods section and Fig. 5) are boxed. Cross bars indicate standard error of the mean. MW, metabolic weight; *, indicates that values (Student-Newman-Keuls test) of the differences with the group receiving soy milk is < 0.01.<p><b>Copyright information:</b></p><p>Taken from "Ability of to overcome host α-galactosidase deficiency, as evidenced by reduction of hydrogen excretion in rats consuming soya α-galacto-oligosaccharides"</p><p>http://www.biomedcentral.com/1471-2180/8/22</p><p>BMC Microbiology 2008;8():22-22.</p><p>Published online 29 Jan 2008</p><p>PMCID:PMC2270848.</p><p></p

Ability of to overcome host α-galactosidase deficiency, as evidenced by reduction of hydrogen excretion in rats consuming soya α-galacto-oligosaccharides-2

water. , Rats associated with DSM10702; , rats associated with a human faecal microbiota; , α-GOS-enriched soy milk (see and ) was added with a 5 % (v/v) coffee bean α-Gal solution at 1 IU/ml and was incubated for 12 h at 37°C; , the concentrations of raffinose and stachyose in the α-GOS-enriched soy milk administered to Cb rats were 48 and 76 mM, respectively; , the concentrations of raffinose and stachyose in the α-GOS-enriched soy milk administered to HMA rats were 144 and 228 mM, respectively; , cultures were at 4 × 10CFU/ml; , α-GOS-enriched soy milk (see ) was added with a 2 % (v/v) inoculum of a 4 × 10CFU/ml CRL722 suspension and was allowed to ferment for 16 h at 37°C.<p><b>Copyright information:</b></p><p>Taken from "Ability of to overcome host α-galactosidase deficiency, as evidenced by reduction of hydrogen excretion in rats consuming soya α-galacto-oligosaccharides"</p><p>http://www.biomedcentral.com/1471-2180/8/22</p><p>BMC Microbiology 2008;8():22-22.</p><p>Published online 29 Jan 2008</p><p>PMCID:PMC2270848.</p><p></p

Ability of to overcome host α-galactosidase deficiency, as evidenced by reduction of hydrogen excretion in rats consuming soya α-galacto-oligosaccharides-0

Olled with a magnetic valve; d, silica gel-containing cylinder to trap moisture; e, KOH-containing cylinder to trap CO; f, peristaltic pump; g, sampling port with syringe. Arrows indicate the direction of air flow through the system.<p><b>Copyright information:</b></p><p>Taken from "Ability of to overcome host α-galactosidase deficiency, as evidenced by reduction of hydrogen excretion in rats consuming soya α-galacto-oligosaccharides"</p><p>http://www.biomedcentral.com/1471-2180/8/22</p><p>BMC Microbiology 2008;8():22-22.</p><p>Published online 29 Jan 2008</p><p>PMCID:PMC2270848.</p><p></p

Ability of to overcome host α-galactosidase deficiency, as evidenced by reduction of hydrogen excretion in rats consuming soya α-galacto-oligosaccharides-1

<p><b>Copyright information:</b></p><p>Taken from "Ability of to overcome host α-galactosidase deficiency, as evidenced by reduction of hydrogen excretion in rats consuming soya α-galacto-oligosaccharides"</p><p>http://www.biomedcentral.com/1471-2180/8/22</p><p>BMC Microbiology 2008;8():22-22.</p><p>Published online 29 Jan 2008</p><p>PMCID:PMC2270848.</p><p></p