Category: Diet

Polyphenols and metabolism

Polyphenols and metabolism

Phytochem Hazelnut benefits — Polyphenolls contribute Mental clarity boosters one of the largest groups of compounds Metabolismm all the phytochemicals. In: Waisundara V, editor. Food intolerance optimization for athletes the feces, the content remained stable during the study and the profile of anthocyanins detected was composed of acylated forms of anthocyanins. Obesity is characterized by chronic, low-grade inflammation which may have a major role in the initiation and development of metabolic diseases. In vitro batch culture of specific probiotic strains. Polyphenols and metabolism

Video

Polyphenols: What They Are, Why They Work, \u0026 How to Eat More of Them - Audio Article

Polyphenols and metabolism -

in the gut microbiota, and hinder the proliferation of pathogenic strains such as Clostridium spp. Polyphenols can also help to control bodyweight by inhibiting appetite, improving lipid metabolism, and inhibiting pancreatic lipase activity 14 , The gut microbiota is able to metabolize polyphenols, making them more bioactive, and easily absorbed than the original compounds 7 , 13 , Both polyphenols and microbiota metabolites may act on metabolic pathways and confer health benefits 19 — Thus, this review aims to provide an overview of data related to the effect of the two-way interactions of polyphenols and gut microbiota in metabolic disorders.

Polyphenols are secondary metabolites of plants, and are widely present in fruit, vegetables, and plant-derived foods such as cocoa, chocolate, tea, coffee, and wine. Polyphenols may influence several metabolic or signaling pathways involved in CVD, T2D, gut health, and cancer Based on their chemical structure and complexity, polyphenols are classified as either flavonoids or non-flavonoids.

Flavonoids have several subclasses: flavones, flavanones, flavonols, flavanols, anthocyanidins, and isoflavones. Non-flavonoid phenolics have a more diverse group of compounds, including phenolic acids, lignans, and stilbenes 22 , 23 Table 1.

Many physicochemical factors may affect the bioavailability, such as polarity, molecular mass, plant matrix, digestibility by gastrointestinal enzymes, and absorption on enterocytes and colonocytes. Bio-accessibility is another important factor in bioavailability Table 1.

Polyphenols characterization, metabolism, and biological activities 13 , 23 — Polyphenols present in foods are generally conjugated with sugars or organic acids, or are present as unconjugated oligomers such as condensed tannins. The released aglycones enter the enterocyte by passive diffusion.

After absorption into the small intestine, aglycones undergo biotransformation in enterocytes and then in hepatocytes. The resultant metabolites are distributed to organs and excreted in the urine.

More complex polyphenols, especially oligomeric, and polymeric structures such as condensed or hydrolysable tannins, reach the colon almost unchanged, where they are metabolized by the gut microbiota together with conjugates excreted into the intestinal lumen through the bile.

Here, they undergo microbial enzyme transformations, including C-ring cleavage, decarboxylation, dehydroxylation, and demethylation. The result is the generation of less complex compounds such as phenolic acids and hydroxycinnamates Several classes of enzymes—such as α-rhamnosidase, β-glucosidase, and β-glucuronidase—are required to deconjugate specific conjugating moieties.

In the case of polymer forms, they are needed to cleave phenolic polymers into individual monomers Once absorbed, polyphenols reach the liver through the portal circulation. They then are distributed to organs and excreted in the urine These compounds undergo microbiota transformation on the colon, generating phenolic acids, and other metabolites Proanthocyanidins produce smaller phenolic acids, such as hydroxybenzoic acids, hydroxyphenylacetic acid, hydroxyphenylpropionic acid, hydroxyphenylvaleric acid, or hydroxycinnamic acids, which can be absorbed Hesperidin and narirutin also pass to the colon, where bacterial enzymes release the aglycone, which is glucuronidated in the intestinal wall.

Aglycones can also be metabolized to phenolic acids. Hydroxyphenylpropionic acid and phenylpropionic acid have been described as the main products of naringenin fermentation. Furthermore, 3- 3-hydroxymethoxyphenyl -propionic acid dihydroisoferral acid , and various hydroxylated forms of phenylpropionic acid have been reported as colonic catabolites of hesperidin Ellagitannins undergo intestinal catabolism, possibly generating ellagic acid, which is metabolized by the microbiota into tetra-, tri-, di- and monohydroxyurolithins The bacteria Gordonibacter urolithinfaciens and Gordonibacter pamelaeae have shown the capacity to biotransformation ellagitannins to urolithins Studies indicate a two-way interaction between phenolics and gut microbiota.

Microbiota may metabolize polyphenols as well as polyphenols and their metabolites may modulate the microbiota by inhibiting pathogenic bacteria and stimulating beneficial bacteria 18 , 33 — Several phenolic compounds have been identified as potential antimicrobial agents with bacteriostatic or bactericidal properties The reciprocal relationship between polyphenols and gut microbiota may contribute to health benefits for the host The gastrointestinal tract is colonized by several bacterial species, mainly the colon.

The mainly microbiota phyla are: Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria , and Verrucomicrobia The composition of the individual microbiota varies in certain circumstances, including diarrheal illness and antibiotic therapy, or induced by nutritional intervention Diet strongly influences the gut microbiota and can modify its impact on health, with either beneficial or deleterious consequences.

Prevotella is the main bacteria in the gut microbial community in people who eat carbohydrate-rich diets, whereas Bacteroides is predominant in the gut of people who follow diets rich in animal protein and saturated fat 36 , Some bacterias are related to the metabolism of polyphenols, especially Flavonifractor plautii, Slackia equolifaciens, Slackia isoflavoniconvertens, Adlercreutzia equolifaciens, Eubacterium ramulus, Eggerthella lenta , and Bifidobacterium spp, which participate in the metabolism of several polyphenols Table 2.

Interindividual differences in the composition of the gut microbiota may lead to differences in the bioavailability and bioactivity of metabolites. These variations are associated with different metabotypes, which are characterized by the individual's ability to produce specific metabolites 25 , 42 , Eubacterium is related to the metabolism of flavonoids, whereas certain species of the genus Bifidobacterium and Lactobacillus are involved in the release of hydroxycinnamic acids in the colon Enterococcus casseliflavus is involved in the hydrolysis of sugar moieties, such as in quercetin O -glucoside, whose process releases the aglycone quercetin and produces lactate, formate, acetate, and ethanol.

Moreover, Eubacterium ramulus, E. oxidoreducens, Flavonifractor plautii and Clostridium strains may metabolize quercetin, leading to the formation of short-chain fatty acids SCFAs , taxifolin, and 3,4-dihydroxyphenyl-acetic acid This could explain why some subjects did not respond to isoflavone intervention to reduce the symptoms of menopause, once the effect was related to equol.

Adlercreutzia equolifaciens, Eggerthella strain Julong , Paraeggerthella hongkongensis, Slackia equolifaciens , and S. isoflavoniconvertens have been identified as able to convert isoflavones to equol Different metabotypes are also observed for ellagitannin and ellagic acid, whose metabolism to urolithins in the gut also shows vast human individual variability associated with differences in the colon microbiota.

Gordonibacter urolithinfaciens sp. was identified and showed the capacity to convert ellagitannins to urolithins 31 , A recent clinical trial by our group to evaluate the bioavailability and metabolism of anthocyanins and ellagitannins showed that the gut microbiota catabolites both classes of polyphenols.

However, some subjects excrete high amounts of polyphenol metabolites in the urine, whereas others excrete low amounts of metabolite.

These findings indicate the high interindividual variability regarding polyphenol metabolism Another recent study 43 showed that pomegranate ellagitannins differently improved CVD biomarkers depending on the individual's urolithin metabotypes UM.

The biomarkers were reduction levels of Tchol, small low-density lipoprotein LDL-c , apolipoprotein apo B, oxidized LDL oxLDL , and non-high-density lipoprotein HDL-c. That is, CVD risk was reduced only in UM-B subjects who displayed an increase in Gordonibacter levels.

Despite these examples, the human gut bacteria involved in most dietary polyphenol transformations remain unknown Weight gain and gut microbiota dysbiosis favor the growth of bacteria that produce isourolithin-A and urolithin-B rather than bacteria that produce urolithin-A 31 , Recently, Selma et al.

The authors concluded that overweight subjects UM-B were at increased risk of cardiometabolic disease, while those with UM-A had greater protection against cardiometabolic factors. Oral consumption of a dose of resveratrol 0. The same study identified two species of bacteria, Slackia equolifaciens , and Adlercreutzia equolifaciens , related to the production of dihydroresveratrol Just as gut microbiota can affect polyphenol metabolism to generate more bioactive metabolites, polyphenols can also affect the microbiota composition.

The mechanisms by which polyphenols modulate the gut microbiota still need to be elucidated, but may involve both direct and indirect interactions.

These compounds can directly stimulate or inhibit bacterial growth. Inhibition refers to the bactericidal or bacteriostatic effect of phenolic compounds, which inhibits the growth of potentially pathogenic bacteria while minimally affecting—or even increasing—the population of beneficial bacteria.

However, it is important to consider the concentration and characteristics of these compounds; that is, the type of compound and whether it occurs in conjugated or free form. Indirectly, phenolic metabolites can affect the growth of one group of bacteria by increasing the development of another group 24 , Resveratrol presented a relevant antibacterial activity on clinically important bacteria, such as Salmonella enterica, Enterococcus faecalis , and Escherichia coli The effects of polyphenols on gut microbiota have been shown in vitro, in vivo and in human studies Table 3.

Table 3. Summary of the main findings of studies related to the effects of polyphenols on gut microbiota and metabolic outcomes. Polyphenols can enhance the abundance of beneficial bacteria such as Bifidobacterium and Lactobacillus which contribute to the gut barrier protection; Faecalibacterium prausnitzii which presents anti-inflammatory action by blocking nuclear factor-kappa B NF-kB activation; and Roseburia sp.

which are butyrate producers Overall, the polyphenol structure, the dosage evaluated, and the strain of microorganism can influence the effect of polyphenols on bacterial growth and metabolism. In this context, Gram-positive bacteria are more sensitive to polyphenols than are Gram-negative bacteria.

This variability might be due to the differences in their wall composition Obesity is characterized by chronic, low-grade inflammation which may have a major role in the initiation and development of metabolic diseases.

Low-grade inflammation increases immune system cell infiltration and the production of inflammatory cytokines in adipose tissue. Polyphenols and their bacterial metabolites can act against obesity by modulating the development of adipose tissue and the obesity-induced inflammatory genes It should be highlighted that most polyphenols inhibit the NF-kB pathway and consequently the expression of inflammatory genes possibly by a mechanism involving microRNAs miRNAs 35 , Polyphenols can modulate more than miRNAs involved in the regulation of different cellular processes such as inflammation and apoptosis In addition, in mice 3T3-L1 adipocytes treated with açaí Euterpe oleracea Martius extract containing cyanidinrutinoside and cyanidinglucoside, there was a reduction in leptin and plasminogen activator inhibitor-1 PAI-1 levels and an increase in adiponectin levels.

This extract also reduced oxidative stress and inhibited the NF-kB pathway Gonzales and Orlando 66 also observed inhibition of the NF-kB pathway and the inflammatory genes expression when adipocytes were treated with curcumin or resveratrol. Other potential anti-obesity mechanisms of polyphenols include inhibition of digestive enzymes and consequently reduce energy efficiency, glucose homeostasis improvement, suppression of adipogenesis and lipogenesis, increase of energy expenditure via thermogenesis, and of fat oxidation, and excretion of fecal lipids Resveratrol, for example, can decrease obesity by reduction of de novo lipogenesis and adipogenesis, increase of adipocytes apoptosis, and oxidation of fatty acids.

Evidence indicates that resveratrol regulates cell-signaling pathways and gene expression These polyphenols downregulated the expression of genes related to adipogenesis and apoptosis adipocyte turnover , energy metabolism, oxidative stress and inflammation Flavonoids can improve glucose homeostasis mainly by the modulation of gene expression that codes key metabolic proteins.

Polyphenols such as green tea polyphenols, cinnamon, and grape seed proanthocyanidins can delay gastric emptying rate and decrease postprandial feeling of hunger by regulating plasma insulin and glucagon-like peptide GLP -1 levels 70 , GLP-1 inhibits glucagon secretion by hampering the gluconeogenesis in the liver and thereby improves insulin sensitivity Moreover, polyphenols such as chlorogenic acid and ferulic acid can upregulate the expression of GLUT-4 and peroxisome proliferator-activated receptor PPAR -γ improving glucose uptake into the cells Polyphenols can interact with cell membranes, changing their structure and function.

They also can interact with cellular receptors, modulate the activities of enzymes and transcription factors, and affect gene expression. Polyphenols are mainly metabolized by the colonic microbiota, forming more bioactive metabolites than those consumed in food.

Along with the modulation of the colonic microbiota, polyphenol-derived metabolites may contribute to host health benefits The gut microbiota helps humans to maximize the absorption of nutrients and energy from the diet, and plays an essential role in physical health status.

Microbial infections and gut microbiota dysbiosis are associated with metabolic disorders Gut microbiota has been considered a potential new contributor to the growing prevalence of obesity and associated cardiometabolic disorders, such as metabolic syndrome, inflammation, and T2D 76 , Subjects with low bacterial richness show increased dyslipidemia, adiposity, insulin resistance, and inflammatory phenotype 7 , 8.

Obese subjects transplanted with the microbiota from lean donors presented increased bacterial diversity in their gut, with an associated increase in butyrate-producing bacteria and subsequent increase in insulin sensitivity The same results were observed in animals.

This phenotype was transferred in germ-free mice transplanted with the microbiota from obese donors 8 , These results can be partly explained by the capacity of the gut microbiota to breakdown undigestible polysaccharides into monosaccharides that could be absorbed, whose fact increased hepatic lipogenesis It should be noted that the gut microbiota can influence energy metabolism and homeostasis.

It does so by regulating the use of energy from the diet, interacting with signaling molecules involved in the metabolism of microorganisms, modifying intestinal permeability, and releasing intestinal hormones—such as peptide YY PYY and GLP-1 Akkermansia muciniphila , a specie increased by polyphenols, was correlated with increased L-cells, the source of GLP-1 and GLP-2 muciniphila was also inversely linked to visceral fat accumulation, adipocyte size in subcutaneous adipose tissue, and fasting plasma glucose levels in obese humans Recent studies have indicated that the gut microbiota produces several metabolites, some of which enter systemic circulation and show biological activity.

The microbiota, through these bioactive metabolites, can act directly or indirectly in organs, with beneficial or adverse effects. Some of the metabolites—such as SCFAs acetate, propionate, and butyrate —may interact with hormones such as ghrelin, leptin, GLP-1, and PYY, which are known to increase satiety and thus reduce bodyweight 46 , During high-fat diet HFD feeding, the microbiota increases gut permeability through mechanisms that involve GLP The result is systemic inflammation, which induces central inflammation via humoral, cellular microglial , or unknown neural pathways.

Energy homeostasis is thus impaired and food intake continues to increase. Moreover, SCFAs, mainly butyrate, are used as an energy source for colonocytes. Also, SCFAs can contribute to several metabolic pathways, including gluconeogenesis propionate and lipogenesis acetate 8. Firmicutes are the main butyrate-producing bacteria in the human gut, especially Clostridium leptum, Faecalibacterium prausnitzii, Roseburia spp.

and Eubacterium rectale. In addition, propionate and acetate are mostly produced by the Bacteroidetes phylum SCFAs can act as signaling molecules and activate several pathways. An example is the activation of the 5' adenosine monophosphate-activated protein kinase AMPK in muscle tissues and in the liver.

AMPK activates key factors involved in lipid and glucose metabolism such as PPARγ, PPARγ coactivator 1 alpha PGC-1α , and liver X receptors LXR AMPK is a sensor of adenine nucleotides that is activated in states of low cellular energy.

In this context, AMPK can stimulate fatty-acid oxidation and mitochondrial biogenesis, which are alternative mechanisms to generate adenosine triphosphate ATP 10 , SCFAs may also act as ligands for G-protein-coupled receptors, also called free fatty-acid receptors GPR or FFAR , in the gut.

These are GPR41 FFAR3 , GPR43 FFAR2 , and GPRA. The result is the suppression of pro-inflammatory cytokine secretion. SCFAs link GPR and GPR, stimulating the secretion of GLP-1 and PYY 8 , 10 , The interaction of butyrate with GPRA reduces the inflammation mediated by interleukin IL -8 and IL and promotes lipolysis in adipose tissue In addition, butyrate may induce fatty-acid oxidation, lipolysis, and thermogenesis, while acetate exerts an anti-lipolytic effect in the WAT, reduces fat accumulation and stimulates mitochondrial activity in the liver 8.

The antilipolytic effect of acetate might be caused by reduced phosphorylation of hormone-sensitive lipase in a GPR-dependent manner 9. AMPK activation induces PGC-1 and SIRT1 expression, which regulates lipolysis-involved cell energy metabolism, and suppresses sterol regulatory element-binding protein 1 SREBP-1 expression, which regulates the genes involved in lipogenesis required for glucose metabolism and fatty acid and lipid production In this context, blueberry polyphenols increased AMPK phosphorylation in liver and WAT and reduced the expression of genes linked to lipogenesis regulation PPARγ, FAS, and SREBP-1 in the liver of mice Resveratrol also decreased the expression of FAS, SREBP-1, and SCD-1 while increased the expression of genes involved in glucose and fatty acids oxidation carnitine palmitoyltransferase CPT -1α, pyruvate dehydrogenase kinase PDK 4 and PPAR-α in obese mice In gut dysbiosis, lipopolysaccharide LPS , a main component of the outer membrane of Gram-negative bacteria, promotes macrophage recruitment and polarization in WAT, inducing inflammation through the Toll-like receptor TLR 4 Figure 1.

LPS binds TLR4 and triggers a cascade of reactions inside the cell that culminates in the release of the NF-kB from the IKK complex and its translocation to the nucleus, activating the inflammatory response.

Increase in plasma LPS levels leads to increased gut permeability, probably due to reduced expression of proteins that compose the tight junction, i. This proteins create a gut epithelial barrier that prevents the bacterial population and products from the gut lumen reaching the blood circulation High LPS concentration in the circulation causes metabolic endotoxemia and induces the production of inflammatory cytokines and mediators such as CRP, which contribute to chronic low-grade inflammation and subsequent cardiovascular risk increase 6.

Figure 1. Metabolic effects of LPS and the effect of polyphenols on beneficial bacteria on enterocytes. A Leaky and inflamed gut. A Western diet, rich in simple carbohydrates sugar , saturated fatty acids, and low in dietetic fiber, may cause obesity-related dysbiosis, and, consequently, loss of gut barrier integrity.

The reduction of mucosal layer thickness and increase in the gut barrier permeability favors the LPS pass through the intestinal cells to the bloodstream, resulting in metabolic endotoxemia. LPS is transported to the target tissues by chylomicrons.

LPS binds to TLR-4 in the target tissue and triggers an inflammatory response. B Normal gut. Dietary polyphenols may sequester reactive oxygen species ROS ; increase Bifidobacterium spp. Thereby, there is a reduction in lipid storage, insulin resistance, and inflammation.

LPS is also linked to impairing pancreatic β-cells by suppressing insulin secretion Metabolic endotoxemia is associated with increased body fat, insulin resistance and increased expression of pro-inflammatory biomarkers Therefore, gut microbiota dysbiosis is involved in various chronic conditions, such as obesity, diabetes, metabolic syndrome, and CVD.

Dysbiosis might also promote the synthesis of SCFAs, which affect the production of cholesterol and fatty acids in the liver, thereby altering the metabolism of lipids Diet has a fundamental influence on the remodeling of the gut microbiota, altering its composition and functionality, which in turn can modulate the susceptibility to disease 86 , Butyrate induces mucus production, which decreases bacterial transport across the epithelium.

It also improves gut integrity by increasing tight junction protein expression Propionate increases intestinal gluconeogenesis 88 , inhibiting the synthesis of hepatic cholesterol; it may also attenuate the secretion of cytokines IL-4, IL, TNF and chemokines 9.

Polyphenols such as resveratrol can increase the Faecalibacterium prausnitzii , which inhibits the NF-kB activation. The greater density of Bacteroidetes has been associated with increased butyrate and propionate levels, which contribute to healthy bodyweight by inhibiting hunger and helping to maintain glucose homeostasis.

Both propionate and succinate were described as efficient substrates for glucose production in the liver 7. Human evidence of a beneficial effect of SCFAs on bodyweight control, inflammation, and insulin sensitivity is increasing, as is evidence regarding its role in glucose and lipid homeostasis 9.

The health properties attributed to beneficial bacteria Bifidobacterium spp. and Lactobacillus spp. for human hosts are manifold. They include nutrient processing, reduction of serum cholesterol, protection against gastrointestinal disorders and pathogens, reinforcement of intestinal epithelial cell-tight junctions, and increased mucus secretion and modulation of the intestinal immune response through cytokine stimulus 25 , 34 , The wide diversity of microbial communities among people can result in vast variability in the composition and functions of the interindividual microbiome 24 , 76 , 86 , 87 , Polyphenols have been compared to prebiotics, since by definition prebiotics are non-digestible polysaccharides.

Polyphenols may protect against diet-induced obesity, although their effects on food intake are controversial. Possibly, polyphenols increase the secretion of mucin and remove reactive oxygen species ROS , creating a beneficial environment for the bloom of the anaerobic Akkermansia muciniphila , and ameliorating metabolic endotoxemia Resveratrol exerts effects on intestinal barrier function and integrity.

Evidence indicates that resveratrol can upregulate the expression of intestinal tight junction proteins muciniphila, Lactobacillus spp.

preserve the integrity of the intestinal mucus and intestinal barrier function, and counteract the deleterious effect of HFD on gut permeability. muciniphila abundance is inversely correlated with bodyweight and with an improved metabolic profile 7 , The abundance of A. muciniphila was found to decrease in obese and diabetic animals and humans 7.

Treatment with A. muciniphila has been suggested to reduce the risk of obesity and related metabolic disorders, because these bacteria have been shown in mice to reverse endotoxemia, inflammation in adipose tissue, gain of adipose mass, and insulin resistance Phenolic metabolites derived from microbial metabolism may exert an anti-inflammatory effect in human health.

Dehydroxylated phenolic acids derived from microbial metabolism of proanthocyanidins reduced the secretion of IL-6, IL-1β, and TNF-α in LPS-stimulated peripheral blood mononuclear cells from healthy subjects Tucsek et al.

The authors found that polyphenol metabolites, such as ferulaldehyde, induced an anti-inflammatory response by reducing MAPK activation, which inhibited NF-κB and ROS production.

Flavonols and proanthocyanidins provided as cranberry extract attenuated HFD-induced obesity and associated metabolic changes. In addition, the extract increased Akkermansia muciniphila , similar to prebiotic administration Branched-chain amino acids BCAA have been shown to be increased in obesity and T2D, contributing to the development of obesity-related insulin resistance.

Possibly, polyphenols from blueberry powder can increase genes for BCAA degradation and consequently improve insulin sensitivity The beneficial effects of polyphenols in humans are still inconclusive.

One reason for that is the high interindividual variation related to polyphenols metabolism and the heterogeneity of individual biological responsiveness to their intake. Most evidence of the anti-obesity effect of polyphenols comes from animal studies 14 , 16 , 21 , Whether animal findings can be extrapolated to humans still warrants further investigation.

Moreover, several in vitro studies have used dietetic polyphenols instead of the bioactive metabolites. Often polyphenols are used at levels above the physiological concentration. It is necessary to establish the concentration of polyphenols in the circulation and tissues, and to perform cell studies using physiological concentrations of the bioactive metabolites.

In addition, more well-designed clinical trials that consider interindividual variation in polyphenol metabolism, and the key role of the microbiota are needed to establish the role of polyphenols in obesity-related metabolic diseases. The association of the microbiome analysis with other omics such as genomics, transcriptomics, proteomics, and metabolomics will be able to clarify the biological effects of the polyphenol-microbiota interactions.

Evidence highlights the importance of the gut microbiota in metabolic diseases such as obesity and T2D, by affecting key pathways such as energy homeostasis and inflammation.

Diet plays a prominent role in modulating the gut microbiota. The two-way interactions between polyphenols and the gut microbiota may contribute to host health benefits. This two-way interaction entails microbial degradation of polyphenols and modulation of gut microbiota by polyphenols and their metabolites, which inhibits pathogenic bacteria and stimulates beneficial bacteria.

Despite the possible benefits of polyphenols for human health through modulating the microbiome, studies have been scarce and present several limitations. The human gut microbiome composition is complex, and the relative proportion of bacteria types varies widely among individuals.

In addition, the metabolome is influenced not only by the gut microbiota but also by genetic and environmental factors. Hence, significant differences in metabolite concentrations may be observed even if subjects consume the same diet. Insight obtained from such integrative studies may also simplify the development of non-invasive diagnostic tools for preventing and treating metabolic diseases, and help to optimize personalized medicine.

TC and MR designed the review. TC wrote the manuscript. MR, NH, and FL revised and approved the manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Van Hul M, Geurts L, Plovier H, Druart C, Everard A, Ståhlman M, et al. Reduced obesity, diabetes and steatosis upon cinnamon and grape pomace are associated with changes in gut microbiota and markers of gut barrier.

Am J Physiol-Endocrinol Metab. doi: PubMed Abstract CrossRef Full Text Google Scholar. Collins B, Hoffman J, Martinez K, Grace M, Lila MA, Cockrell C, et al. A polyphenol-rich fraction obtained from table grapes decreases adiposity, insulin resistance and markers of inflammation and impacts gut microbiota in high-fat-fed mice.

J Nutr Biochem. Pan MH, Wu JC, Ho CT, Lai CS. Antiobesity molecular mechanisms of action: Resveratrol and pterostilbene. Rogero MM, Calder PC.

Obesity, inflammation, toll-like receptor 4 and fatty acids. Dao MC, Clément K. Gut microbiota and obesity: concepts relevant to clinical care. Eur J Intern Med. González-Sarrías A, Romo Vaquero M, García-Villalba R, Cortés-Martín A, Selma MV, Espín JC.

The endotoxemia marker lipopolysaccharide-binding protein is reduced in overweight-obese subjects consuming pomegranate extract by modulating the gut microbiota: a randomized clinical trial.

Mol Nutr Food Res. Eid HM, Wright ML, Anil Kumar NV, Qawasmeh A, Hassan STS, Mocan A, et al. Significance of microbiota in obesity and metabolic diseases and the modulatory potential by medicinal plant and food ingredients. Front Pharmacol.

Cani PD, Van Hul M, Lefort C, Depommier C, Rastelli M, Everard A. Microbial regulation of organismal energy homeostasis. Nat Metab.

CrossRef Full Text Google Scholar. Canfora EE, Meex RCR, Venema K, Blaak EE. Gut microbial metabolites in obesity, NAFLD and T2DM. Nat Rev Endocrinol. Gérard P. Gut microbiota and obesity.

Cell Mol Life Sci. Al-Assal K, Martinez AC, Torrinhas RS, Cardinelli C, Waitzberg D. Clin Nutr Exp. Meijnikman AS, Gerdes VE, Nieuwdorp M, Herrema H. Evaluating causality of gut microbiota in obesity and diabetes in humans.

Endocr Rev. The profile of natural polyphenols and their yield in biota is affected by postharvest treatment and processing technology. Wei et al. revealed that 0. Moreover, different processing treatment of sea buckthorn leaves were examined phytochemically, including fresh leaves, black tea produced by withering, rolling, fermentation and drying, and green tea produced by rolling, screening and drying process.

Significant differences of polyphenol patterns occurred among the different processing tea Wang et al. The fermentation process makes the polyphenols susceptible to oxidation by enzymes, allowing catechins to be converted into theaflavins and thearubins, which confer the black tea fragrance and color.

In summary, the above-mentioned results demonstrate a valuable aspect to the composition, characterization, and bioactivities of natural polyphenols from fruit and traditional plants, in the context of preventing or controlling metabolic syndrome-associated diseases, especially obesity and diabetes.

Polyphenols have a wide range of benefits and pharmacological effects. This reiterates that they serve as promising nutraceuticals or pharmaceuticals in health and food industries.

Despite the evidence that has accumulated in relation to this important Research Topic, there are still many aspects that need to be clarified and improved. For example, low bioavailability of many polyphenols limits their application on food industry or the clinic.

There are key techniques that may improve their bioavailability, such as formation of micelles, nanoparticles, liposomes, and phospholipid complexes.

Converting polyphenols into ingredients that can be easily utilized through gut microbiota could be another way to promote the utilization of polyphenols Chen et al. All authors listed have made a substantial, direct, and intellectual contribution to the work and approved it for publication.

This research was supported by National Key Research and Development Program YFF and the National Natural Science Foundation of China and The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Saklayen MG. The global epidemic of the metabolic syndrome.

Curr Hypertens Rep. doi: PubMed Abstract CrossRef Full Text Google Scholar. Engin A. The definition and prevalence of obesity and metabolic syndrome. Adv Exp Med Biol. Gierach M, Gierach J, Ewertowska M, Arndt A, Junik R. Correlation between body mass index and waist circumference in patients with metabolic syndrome.

ISRN Endocrinol. Yang H, Xiao L, Yuan Y, Luo X, Jiang M, Ni J, et al. Procyanidin B2 inhibits NLRP3 inflammasome activation in human vascular endothelial cells. Biochem Pharmacol. Yang H, Tuo X, Wang L, Tundis R, Portillo MP, Simal-Gandara J, et al.

Bioactive procyanidins from dietary sources: The relationship between bioactivity and polymerization degree. Trends Food Sci Tech. Liu D, Deng J, Joshi S, Liu P, Zhang C, Yu Y, et al. Monomeric catechin and dimeric procyanidin B2 against human norovirus surrogates and their physicochemical interactions.

Food Microbiol. Fan W, Zong H, Zhao T, Deng J, Yang H. Bioactivities and mechanisms of dietary proanthocyanidins on blood pressure lowering: A critical review of in vivo and clinical studies.

Laura Polyphenols and metabolism PolyphenilsLuke R. E-mail: franck. Metabolsm wsu. Berries are rich in phenolic compounds such Hazelnut benefits phenolic Selenium test scripts, flavonols and anthocyanins. These molecules are often reported as being responsible for the health effects attributed to berries. However, their poor bioavailability, mostly influenced by their complex chemical structures, raises the question of their actual direct impact on health. Anx on the Research Metabolidm Natural polyphenols and Anti-aging skincare techniques syndrome. Metabolic syndrome is a chronic disease All-around wellness benefits by Mental clarity boosters, obesity, Hazelnut benefits, and hyperlipidemia, as metaboljsm by the World Health Ketabolism 1. Mental clarity boosters risk factors, including an unhealthy diet, Healthy calorie intake, Hazelnut benefits environmental factors, Poyphenols the chances of metaholism metabolic metabolis. Mental clarity boosters, intervention does meetabolism only involve exploring clinical therapeutic treatment at the point of diagnosis, but it is also crucial to prevent the occurrence of metabolic syndrome and its complications by keeping a healthy lifestyle, such as by doing sports or by adding vegetables, low sugar fruit, and less salt to the diet. Natural polyphenols, common specialized metabolites from plants, are a class of bioactive compounds widely found in fruits, vegetables, tea, and herbal medicines. They confer potentially beneficial activity, by regulating gut microbiota and enacting anti-inflammation or antioxidation 4 — 6. A diet rich in polyphenols alleviates the symptoms and risk factors of metabolic syndrome, such as by reducing blood pressure, improving insulin-resistance and modulating lipid metabolism 78.

Author: Tygomuro

3 thoughts on “Polyphenols and metabolism

Leave a comment

Yours email will be published. Important fields a marked *

Design by ThemesDNA.com