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 non-absorbed polyphenols are subjected to bio-transformation via the activity of enzymes from various microbial groups . Consequently, the micro-biota-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,nft channel the functional capability of the gut micro-biota 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 low phytochemical, 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.200 Overall, the direct effects of fiber blur the ability to judge the specific effects of individual dietary ingredients on gut micro-biota. These dietary ingredients may act in an additive or a synergistic manner, exerting their effects on gut micro-biota. The prebiotic-like flavonol-rich foods have been demonstrated to modify the composition of gut micro-biota. 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 inter individual 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 micro-biota 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. More comprehensive human intervention studies will be essential in the future to provide insight into the potential influence of dietary polyphenols and their aromatic bacterial metabolites on intestinal microbial communities and their activities.Probiotics are defined as viable microorganisms that, when consumed in sufficient amounts, confer a health benefit on the host.To date, most of the commonly used probiotics are limited to strains of certain Lactobacillus and Bifidobacterium species .
Survival during passage through the GI tract is generally considered as the essential feature for probiotics to preserve their active functions in the colon. Indeed, the probiotic strains must overcome biological barriers, including resisting gastric and bile acid secretion and tolerating intestinal lysozyme and toxic metabolites produced during digestion . Various studies found that at least a fraction of probiotic bacteria can be detected in stool for between 1 and 3 weeks after consumption . Probiotic Lactobacillus strains were also found to adapt for survival in the gut and possess gut-inducible genes that are responsive at different sites in the intestine.Interestingly, provision of the probiotic Lactobacillus plantarum to mice fed a Westernstyle diet and to humans resulted in similar gene expression profiles of this strain.As probiotics are delivered via various food vehicles, the complex food matrix should also be viewed as an important factor that may alter the probiotic activity in the gut. To date, only a few animal and clinical studies have addressed the functional roles of food on probiotic-conferred health benefits.The mechanisms of probiotic effects on health are only partially understood but likely function either directly through interactions with host intestinal epithelial and immune cells or indirectly by modulating the indigenous intestinal micro-biota. In regard to the latter, several studies have concluded that probiotic consumption does not result in global modifications of the intestinal micro-biota in healthy individuals.However, probiotics might confer modest but significant changes to the functional activities of local intestinal bacterial populations. When examined at the meta-transcriptional level, intake of a probiotic fermented milk was associated with the upregulation of microbial genes corresponding to plant polysaccharide metabolism.Similarly, administration of probiotics was shown to induce crosstalk between the probiotics from the diet and the individual bacterial species in the gut and might induce competition for limited substrates that results in fluctuations tof the metabolic profile of the host.The gut micro-biome of healthy adults is highly resilient , where the stable native micro-biota prohibits the succession of microbes from the diet.In addition, the effect of probiotics on the gut micro-biome appears to differ depending on host phenotypes such as age, health status, and chronic conditions. For example, the infant gut micro-biome is highly diverse and dynamically changes during development and therefore may be easily influenced by the consumption of probiotics . In individuals with irritable bowel syndrome , probiotic consumption resulted in an increase in the numbers of Bacteroidetes in the intestine.Moreover,hydroponic nft intake of two Lactobacillus strains by diet-induced obese mice altered microbial composition and decreased expression of inflammatory genes in the adipose tissue while increasing levels of fatty acid oxidation in the liver.Further studies are needed to investigate the effects of assorted probiotic supplements on the gut micro-biome with respect to various host life stages and phenotypes.
The premise behind substituting sugar with artificial sweeteners is to maintain the palatability of food at the same time as lowering energy intake. However, a sufficiently high ingestion of non/low-digestible sugar substitutes stimulates the growth of gut micro-biota and can induce transitory diarrhea in humans.In particular, the great proportion of non/lowdigestible sugar substitutes that reach the distal intestine are subject to fermentation by the colonic micro-biota, offering approximately 2 kcal/g of energy.Although discovering and characterizing these compounds within foods is relatively new, it is of interest to note that many of these food ingredients are common in our daily diet. For example, the disaccharide alcohol maltitol is considered a common replacement for sucrose. Urinary and fecal excretions of sorbitol and maltitol after 24 h in conventional rats were shown to be minimal compared with germ-free rats.Likewise, maltitol consumption significantly increased production of SCFAs in addition to nine tested fecal microbes after a 6 week trial, including bifidobacteria, Bacteroides, Clostridium, lactobacilli, eubacteria, Atopobium, Fusobacterium prausnizii, Ruminococcus flavefaciens, and R. bromii. A 12 week administration of Splenda, composed of 1.1% of the artificial sweetener sucralose, increased fecal pH and reduced the amount of fecal bifidobacteria, lactobacilli, Bacteroides, clostridia, and total aerobic bacteria in a rat, whereas isomalt, a widely used low-energy sweetener, was considered to be bifidogenic in a human study.Overall, artificial sweetener fermentation by gut micro-biota remains either unexplored or poorly documented, some of which are highlighted in a review by Payne et al..Azo compounds are widely used as coloring agents in foods, beverages, and food packaging.In addition, azo polymer coatings have been specifically designed for colon-selective drug delivery due to the presence of pH-sensitive monomers and azo cross-linking agents in the hydrogel structure.Indeed, azo dyes can be metabolized under anaerobic conditions by intestinal microbial processes and, as a result, produce the reductive cleavage products aromatic amines . The majority of the toxic effects of azo dyes are exerted through aromatic amines produced by their colonic degradation.Raffi et al. reported that isolated intestinal bacteria in an anaerobic culture system were able to decolorize the dyes in the supernatant, suggesting that some of the azoreductase activities are extracellularly released.Xu et al. demonstrated a variable degree of efficiency in the reduction of Sudan azo dyes and Para Red by 35 prevalent human intestinal microbes in vitro.In contrast, Sudan azo dyes and their metabolites selectively inhibit the growth of some human intestinal microorganisms,which may suggest a potential impact on gut micro-biome after long-term exposure. In summary, although there are tantalizing glimpses into the effect of azo dyes on microbes in vitro, more data from animal and human studies are keenly awaited.In the colon, sulfur is present in either inorganic form or organic form .The human GI tract poorly absorbs sulfate, and there is little sulfatase activity in the mucosa of the GI tract; therefore, free sulfate in the colon is likely to be of dietary origin.Dietary sulfate drives the activity of sulfate-reducing bacteria that couple oxidative phosphorylation with reduction of sulfate to produce sulfide.The total inorganic sulfur intake is much higher in the Western diet in comparison to a typical African rural diet. Highly processed foods that are high in sulfate include bread, soy flour, dried fruits, and brassicas, as well as sausage, beers, ciders, and wines.Sulfur-containing amino acids such as cysteine can be found in dietary protein and are a source of sulfur for colonic sulfate-reducing bacteria Desulfovibrio desulfuricans.Native Americans who consume a diet high in resistant starch and low in animal products harbor significantly distinct sulfate-reducing bacterial populations and more diverse and different methanogenic archaea than Americans consuming a typical Western diet.Substrate competition for hydrogen among methanogenic archaea, sulfate-reducing bacteria, acetogenic bacteria, and otherspecies likely occurs in the colon.Because hydrogen is an essential component for the survival of colonic methanogens, removal of the substrate terminates methanogenesis. Given an adequate supply of sulfate, sulfate-reducing bacteria that are more abundant in the right colon outcompete methanogenic archaea for H2 due to their higher substrate affinity to produce hydrogen sulfide , an end-product of dissimilatory sulfate reduction.As a result, the mucosal micro-biome may be shaped in part through the availability of toxic sulfide compounds and the differential susceptibility of mucosalistic microbes to the toxins.Furthermore, the activity of methanogenic bacteria can also be disrupted by bile acids. In brief, methane production was thought to occur only when sulfate-reducing bacteria were not active.If sulfate is limited and hydrogen is in relative excess, methanogenic bacteria or perhaps acetogenic bacteria will become essential.Therefore, the levels of sulfate present in the colon are critical for determining which bacterial group gains a better survival advantage.Alcohol. Many people consume alcoholic beverages; however, few studies exist on the effect of alcohol consumption on the gut micro-biome of healthy individuals. For individuals who consume alcohol to excess, abnormal gut micro-biota and bacterial overgrowth can potentially initiate or worsen alcohol induced impaired gut barrier function and contribute to endotoxemia in patients with alcoholic fatty liver disease.