The effect of dietary fiber has long been proposed to contribute to human health through prebiotic enhancement of certain beneficial microbes that produce butyrate,absorb bile acids,decrease colon pH,112 and promote GI motility via shortening of the mean transit time.However, not all dietary fibers have the same effect, which is dependent on their physicochemical characteristics.The prebiotic effect of indigestible polysaccharides on gut microbiota has previously been broadly discussed. Several human dietary intervention studies have shown that intake of certain types of dietary fibers can significantly modify the gut microbiota observed in feces. For example, consumption of whole-grain breakfast cereal for 3 weeks significantly increased fecal bifidobacteria and lactobacilli compared to wheat bran alone; however, no difference was observed in fecal short-chain fatty acids .Introduction of barley β-glycan in the diet elevated fecal Bifidobacterium and Bacteroides counts in older healthy human subjects , whereas only the Clostridium perfringens count increased in the younger group.Typically, consumption of nondigestible carbohydrates such as wheat bran arabinoxylan oligosaccharides, short-chain fructooligosaccharides , and soybean oligosaccharides and galactooligosaccharides induces enrichment of human fecal bifidobacteria.Inulin has been shown to stimulate the growth of Bifidobacterium adolescentis, Bifidobacterium longum, Bifidobacterium bifidum and the butyrateproducing bacteria Faecalibacterium prausnitzii and Roseburia inulinivorans. Similarly, Bifidobacterium spp. levels significantly increased upon consumption of biscuits containing partially hydrolyzed guar gum and FOS for 21 days, whereas Bacteroides spp., Clostridium spp., and Lactobacillus−Enterococcus spp. remained at similar levels.

GOS alone or combined with FOS are often supplemented in infant formula to favor the growth of bifidobacteria spp.,drainage planter pot and the bifidogenic response of GOS has been shown to be dosedependent.Interestingly, Rossi et al. reported that only 8 of the total 55 Bifidobacterium strains were able to grow on longchain inulin in vivo,suggesting that not all bifidobacteria species benefit in the same way from the presence of these substrates as their energy source. Indeed, the specificity of polysaccharide use by the gut microbiota supports the underlying cross-feeding interaction between gut microbiota . Various types of resistant starch demonstrate substrate specialization of the gut microbiome. For example, the impact of type 2 resistant starch is associated with enrichment of Ruminococcus bromii, whereas type 3 resistant starch elevates both E. rectale and R. bromii in healthy130 and overweight subjects.Type 4 resistant starch significantly differs from types 2 and 3 and has been shown to induce a profound phylum-level change and elevate B. adolescentis and Parabacteroides distasonis. Furthermore, the variability observed in these studies suggests that the host-specific environment affects the composition of the gut microbiome. The fermentation profile depends on the glycosidic linkage type of the dietary substrate as well as the functional capability of the gut microbiota . Metatranscriptome analysis revealed a functional enrichment of genes associated with carbohydrate uptake and metabolism in the small intestine and feces.A fecal metaproteomic analysis from three healthy subjects over a period of 6−12 months revealed a common functional core enriched in carbohydrate transport and degradation.In particular, the ability to degrade complex polysaccharides has been identified in a range of bacteria.In particular, the Bacteroides phylum contains a large repertoire of genes that exhibit broad capacities to degrade a great diversity of plant-derived polysaccharides.Microbial sequencing projects revealed that starch utilization systems are highly abundant and conserved in the phylum Bacteroidetes .

In contrast, members from the Firmicutes phylum exhibit a wide range of functionalities; for example, Ruminococcus, which is in the order of Clostridiales, can degrade cellulose and pectin,whereas E. rectale and Eubacterium eligens have fewer polysaccharide degrading enzymes and are enriched with more ATP binding cassette transporters and phosphotransferase systems than the Bacteroidetes.Although many microbes have the ability to ferment undigestible dietary components, diet-induced microbial changes seem to favor the groups that have a stronger survival advantage and perhaps specifically depend on host-derived factors such as pH and bile acid profiles.The human colon has not often been considered to be a site of fat absorption; however, the small intestine absorbs only approximately 95% of dietary lipids after consumption of a typical Western diet.Furthermore, some studies have suggested that colonic absorption of medium-chain fatty acids takes place in dogs,rats,and humans and that glycerol accumulates in the colon when fat absorption is disturbed in the small intestine.Accumulation of glycerol has been shown to alter the Lactobacillus and Enterococcus communities in the gut.A diet high in animal fat and low in dietary fiber stimulates the synthesis and enterohepatic circulation of primary bile acids.Although the majority of bile acids are recycled in the ileum, some of them escape the enterohepatic circulation in the intestine and become substrates for microbial metabolism in the colon.Bile acids restrict the growth of several microbes.Accordingly, only the microbes that are able to tolerate the physiologic concentrations of bile acids survive in the gut; thus, bile acids appear to exert strong selective pressure on gut microbial structure and function. For example, administration of cholic acid to mice induces phylum-level population shifts of the relative abundance of Firmicutes and Bacteroidetes that resembles microbial changes observed by feeding a high-fat diet alone.Gut microbiota detoxify primary bile acids via deconjugation, in which well-conserved bile salt hydrolases release the amino acids glycine and taurine.

The free primary bile acids are then converted into various types of secondary bile acids such as deoxycholic acid and lithocholic acid by the 7α- dehydroxylation reaction.A detailed list of bacteria with genes encoding bile salt hydrolase activity is reviewed by Ridlon et al.In general, the conjugated bile acid profile is heavily dependent on microbial activity. The bile acid distribution profile in multiple compartments of germ-free animals shows less diversity and is smaller in size compared with conventional counterparts.Dietary lipid composition can also modulate bile acid profile, in particular, increasing taurocholic acid that, as a consequence, promotes the growth of Bilophila wadsworthia, a Gram-negative opportunistic pathogen.B. wadsworthia utilizes taurine as a source of sulfite,which serves as the terminal electron acceptor for the respiratory chain.The concentrations of bile acids and their conjugation status to glycine or taurine between individuals may be influenced by diet, as people eating a meat-rich diet tend to have more taurine-conjugated bile acids in their bile acid pool than those eating a vegetarian diet.It has been recognized that the production of secondary bile acids is pH dependent. The proximal colon is more acidic than the distal colon,which results in an elevated activity of 7α-dehydroxylase in the cecum versus the left colon.Subjects consuming diets high in resistant starch showed a significantly decreased stool pH compared with subjects consuming a low resistant starch diet. A decrease in pH is associated with an elevated production of SCFAs, which selectively regulate the intestinal microbial community, with a tendency to suppress Bacteroides spp.and promote butyrate-producing Gram-positive bacteria such as E. rectale. Similarly, subjects on a vegan or vegetarian diet showed significantly more acidic stool pH89 and significantly lower fecal secondary bile acid production83 than omnivores. Higher consumption of animal protein is one possible explanation of higher fecal pH value in an omnivorous diet, as proteolytic putrefactive bacteria are able to increase stool pH by producing alkaline metabolites. Thus, increases in SCFAs result in a more acidic colonic pH, a decreased solubility of bile acids, an indirect increased absorption of minerals, and a reduction of ammonia absorption, which indirectly alters the composition of gut microbiota.Importantly, 50−70% of acetate taken up by the liver becomes the primary substrate for cholesterol synthesis, whereas propionate inhibits cholesterol synthesis in hepatic tissue . Therole of cholesterol on gut microbiota was first elucidated using germ-free rats. Danielsson et al. demonstrated that germ-free rats exhibit a higher serum cholesterol level than their conventional counterparts.More recently, the characterization of the gut microbiota in a hamster model of hypercholesterolemia showed that dietary intervention with grain sorghum lipid extract180 modulated the gut microbial composition, with bifidobacteria being positively associated with increases in HDL cholesterol level and the family Coriobacteriaceae being associated with non-HDL cholesterol.Together, high intake of dietary fat, in particular animal fat, and cholesterol not only changes the composition of bile acids and neutral sterols in the colon but also modifies the gut microbiota,plant pot with drainage which consequently transforms these compounds into secondary bile acids and cholesterol metabolites.Polyphenols present in a wide range of plant-based foods have received great interest owing to their antioxidant capacity and potential protective effect in reducing cardiovascular disease risk through improvement in vascular function and modulation of inflammation. The interpretation of the influence of polyphenols on cardiovascular health in dietary intervention studies can be complicated due to dynamic bio-availability during the processes of absorption, metabolism, distribution, and excretion. Generally, the absorption of dietary polyphenols is widely dependent on the type and structure of the compound and is often slow and largely incomplete in the small intestine. Therefore, significant quantities of polyphenols are retained in the colon. In addition, the nonabsorbed polyphenols are subjected to biotransformation via the activity of enzymes from various microbial groups . Consequently, the microbiota-derived metabolites of polyphenols are better absorbed in the gut,which then become an important factor in the health effect of polyphenol-containing foods. Important plant polyphenols and their microbial derivatives are listed in ref.

Many of the studies that assess bio-availability and effects of polyphenols have evaluated the balance between the enterohepatic circulating levels, residence time in plasma, and urine excretion rate of the parent phenolic compounds and their microbial-derived metabolites using metabolomic techniques.Importantly, although endogenous enzyme and transporter activities in the small intestine as well as transformation of polyphenols are subject to a wide inter individual variability, the functional capability of the gut microbiota is important to partially explain the variation of bio-availability among the population.Assessing the properties of a single dietary constituent from the polyphenol family alone without dietary fiber is difficult due to the complex dietary food matrix present in a flavonoid-rich diet. For example, regular consumption of apples increased the numbers of fecal bifidobacteria and decreased the C. perf ringens count.Similarly, the concomitant dietary presence of apple polyphenols and FOS increased SCFA production.In contrast, compared to consumption of an inulin-containing diet alone, including a grapefruit flavonoidrich extract decreased both production of SCFAs and the bifidobacteria population.Furthermore, a randomized crossover intervention study in which subjects consumed high levels of cruciferous vegetables for 14 days revealed an alteration of the fecal microbial community profile compared with a lowphytochemical, low-fiber diet, including a higher abundance of Eubacterium hallii, Phascolarctobacterium faecium, Burkholderiales spp., Alistipes putredinis and Eggerthella spp.The observed changes could also be explained by the increase in dietary fiber that is enriched in cruciferous vegetables.Overall, the direct effects of fiber blur the ability to judge the specific effects of individual dietary ingredients on gut microbiota. These dietary ingredients may act in an additive or a synergistic manner, exerting their effects on gut microbiota. Six week consumption of a wild blueberry drink that was high in polyphenols was shown to increase the proportion of Bifidobacterium spp. compared to the placebo group;however, a high interindividual variability in response to the dietary treatment was also observed.Similarly, the daily consumption of a high-cocoa flavonol drink for 4 weeks significantly enhanced the growth of fecal bifidobacterial and lactobacilli populations, but decreased the Clostridia histolyticum counts relative to those consuming a low-cocoa flavonol drink .Furthermore, unabsorbed dietary phenolics and their metabolites selectively inhibit pathogen growth and stimulate the growth of commensal bacteria. For example, grape pomace phenolic extract increases Lactobacillus acidophilus CECT 903 growth in liquid culture media.In addition, upon bacterial incubation, tea phenolics were shown to suppress the growth of potential pathogens such as Clostridium spp. and Gram-negative Bacteroides spp., whereas commensal anaerobes such as Bifidobacterium spp. and Lactobacillus spp. were less affected.Similarly, the flavanol monomer -catechin significantly increases the growth of the Clostridium coccoides−Eubacterium rectale group, Bifidobacterium spp., and E. coli and significantly inhibits the growth of C. histolyticum group in vitro.To date, there is a wide range of phenolic compounds that have been demonstrated to have antimicrobial properties,and many have been previously reviewed.Although many of the studies highlighting the beneficial role of plant polyphenols through regulation by gut microbiota appear promising, there are limitations in the results that can be drawn regarding the ability of flavonoids to influence the growth of selected intestinal bacterial groups using a batch-culture model.