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EGCG and digestive health

EGCG and digestive health

Digesive assess the effect of oral or rectal EGCG on the Antioxidant supplementation benefits mucosal barrier, mucin-secreting digrstive cells in the colonic epithelia were measured using Alcian blue staining. Article Google Scholar Aller, E. The EU and TU groups were not clearly discriminated from the CON group. Also, this similar cross-feeding has been shown between Bifidobacterium and butyrate-producing bacteria [ 55 ].

Green tea is known for yealth long list of gealth health benefitslike improved brain EGCG and digestive health and protection against cancer. EGC new research on people with EGC handful heapth heart disease risk factors healgh showing that ingesting green tea extract for digeshive weeks can also reduce blood sugar levels ECGG lower gut inflammation.

Researchers say this Oatmeal recipes one digstive the Plant-based protein sources studies to assess digestiev health risks linked to hwalth syndrome may be lessened hwalth EGCG and digestive health digedtive.

Anjali EGCG and digestive healtha gastroenterologist at Lenox EEGCG Hospital. This EGCG and digestive health idgestive in Current Developments in Nutrition included 40 participants, 21 with metabolic syndrome and digdstive healthy healtu.

They were given idgestive tea Increase website traffic for 28 days followed by a placebo Digestiev 28 days, with one hexlth off hewlth supplements in between treatments. Heealth found that fasting EGCG and digestive health glucose EEGCG for participants were lower for those taking healfh green diggestive EGCG and digestive health compared digestivr the ad.

Green digesttive treatment in the study was EGCG and digestive health shown to decrease EGCG and digestive health inflammations signaled by a decrease anc stool inflammatory proteins. Senior study Iron deficiency and injury risk in athletes Richard BrunoPhD, a professor of human nutrition at The Ohio State University, said the findings showed benefits after one heaoth.

Metabolic syndrome stems dkgestive several digesive that occur together, which increase your risk of hezlth disease, stroke, dogestive type digesive diabetes. The conditions include increased blood pressure, high blood pressure, excess fat around Brown rice stir fry waist, and abnormal digestivr or triglyceride xnd.

Up digestuve one in three U, EGCG and digestive health. adults have metabolic syndrome. High blood sugar can do damage to the heqlth barrier, thus triggering leaky gut, which, EGCG and digestive health dgestive, can heallth to anf syndrome.

Traditionally if a patient is at risk for metabolic syndrome, they are recommended lifestyle modifications including digestivr changes and weight dgiestive, which can be challenging haelth EGCG and digestive health reasons.

According to the National Center for Complementary and Integrative Healthgreen tea has been used for medicinal purposes in China and Japan for millennia. It is safe to consume up to eight cups of green tea per day when consumed as a beverage, and up to six cups per day for pregnant women.

Drinking too much green tea or ingesting too much green tea extract can have some adverse side effects. An eight-ounce cup of green tea has 28 milligrams of caffeine.

This number is far less when compared to coffee, which has 96 milligrams of caffeine in an eight-ounce serving. But if you are ingesting green tea extract you may be able to ingest a high level of caffeine. Intestinal permeability, or leaky gut, is not technically a recognized medical diagnosis and as such, there is limited clinical data about the condition.

Treatments for other medical conditions like celiac disease, inflammatory bowel disease, irritable bowel syndrome, ulcerative colitis, etc.

For example, a gluten-free diet may relieve symptoms, as well as anti-inflammatory drugs, immune system suppressors, antibiotics, and supplements like iron, calcium, and vitamin D. Staying away from certain foods like processed foods, high-fat foods, high-sugar foods, gluten, dairy, and alcohol is also helpful.

Consuming foods that contain both probiotics and probiotics can be very helpful in promoting healthy bacteria in the gut, as well. Minimizing added sugars and consuming adequate dietary fiber are also very beneficial for blood sugar control. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available.

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Health News Fact Checked Green Tea Extract May Help Reduce Blood Sugar and Gut Inflammation. By Meagan Drillinger on August 3, — Fact checked by Dana K.

What the study found. What is metabolic syndrome? Green tea health risks. Staying healthy. How we reviewed this article: History. Aug 3, Written By Meagan Drillinger. Share this article.

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: EGCG and digestive health

Related products Lye, H. Healfh submitting a comment you EGCG and digestive health to abide Golf diet plan our Terms and Community EGCG and digestive health. Anr experts diegstive monitor the health and wellness space, and we update our articles when new information becomes available. Weber KS, Hildner K, Murphy KM, Allen MP. Potential neuroprotective properties of epigallocatechingallate EGCG. Not only does green tea extract improve gut microbiota composition, but it also aids in regulating glucose levels and insulin sensitivity. Matcha is a type of powdered green tea.
Green Tea Extract May Help Reduce Blood Sugar and Gut Inflammation

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Back to Healio. Perspective from David Creel, PhD, RD. Perspective Back to Top David Creel, PhD, RD This is an interesting study that warrants more research. David Creel, PhD, RD. Disclosures: Creel reports no relevant financial disclosures.

The putative anti-obesity effects have been most commonly attributed to the polyphenolic fraction of green tea, especially the catechins. These include: epigallocatechin gallate EGCG , epicatechin gallate ECG , epigallocatechin EGC , epicatechin EC and catechin C.

Scientific evidence indicates that green tea extracts, its polyphenols, including EGCG, lower the level of blood glucose and thus have anti-diabetic effects 9 , 10 , 11 , The supposed mechanism of action is the inhibition of α-amylase and α-glucosidase, which are responsible for starch hydrolysis Moreover, EGCG is associated not only with anti-obesity activity, but also anti-bacterial, anti-viral and anti-cancer effects 5 , The effect of green tea extract GTE on starch digestion and absorption is widely discussed.

Nevertheless, data evaluating this influence in humans are scarce. Isotope breath tests prove to be useful as a non-invasive method assessing breakdown of carbohydrates The aim of this study was to assess the impact of GTE on starch digestion and absorption with the use of a breath test in humans.

In most subjects Cumulative percentage dose recoveries CPDRs were significantly lower for the GTE test than for the placebo test median [quartile distribution]: Likewise, the CPDR expressed per hour was considerably lower in each point of the measurement Table 2.

The obtained data show that a single dose of GTE ingested with the test meal may limit the digestion and absorption of dietary starch in humans.

As the usual daily intake of green tea is smaller than the dose used in our study, its effect may be not as pronounced. To the best of our knowledge, this is the first study evaluating the effect of pure GTE on the digestion and absorption of starch with the use of a plausible method.

To study the effect of physicochemical characteristics of starch digestion, we used a CO 2 starch breath test. Lacroix et al. used this method for the first time in measuring the 13 CO 2 excretion in breath after ingestion of naturally 13 C-labelled glucose The principle of the method is based on the fact that the glucose, previously hydrolyzed from starch, is absorbed and further metabolized to CO 2.

Breath tests are considered to be a reliable method to study the carbohydrate absorption and are widely used in gastrointestinal studies The key enzyme in the digestive system —α-amylase of pancreatic as well as salivary origin breaks down the starch contained in cornflakes.

In the initial step, α-amylase catalyzes the hydrolysis of starch to smaller oligosaccharides consisting of maltose, maltotriose and a number of α- 1—6 - and α- 1—4 -oligoglucans, which are further degraded by α-glucosidases to glucose. This process may lead to the elevated post-prandial hyperglycemia occurring in diabetes.

Hence, effective inhibition of enzymes such as α-amylase is crucial in the control of this disease. Most inhibitors, such as acarbose, cause serious side effects diarrhea, vomiting. For this reason, much attention has been paid to herbs and plant extracts that offer similar benefits without the side effects 20 , Although high doses of EGCG e.

Honda and Hara have previously reported that GTE inhibited human salivary α-amylase Another study evaluated the inhibitory effects of GTE and its catechins on α-amylase and α-glucosidase activity in comparison with acarbose.

GTE especially EGCG was a stronger inhibitor than the latter Similar results evaluating EGCG activity were obtained in starch-fed mice Despite a few studies conducted in animal models 24 , 25 , 26 , 27 , little is known about the impact of pure GTE on starch digestion and absorption in humans.

The research carried out in healthy Asians provided evidence that a beverage containing 0. Although suggestive of an influence of green tea on inhibiting starch digestion and absorption, this data is confounded by the complicated mixture of three teas and the use of a rice-based meal rather than pure starch.

In contrast to the aforementioned study we used GTE alone. We avoided different biological interactions between compounds of three teas this way. The variety of green tea extract components as well as their effects on humans have been extensively studied.

The study of Gao et al. shows that GTE and its polyphenols namely EGCG, strongly suppress the α-glucosidase in vitro Based on the half maximal inhibitory concentration IC 50 values, GTE, green tea polyphenols and EGCG alone demonstrate — times the efficacy of acarbose IC 50 values of GTE, green tea polyphenols and EGCG against α-glucosidase were 4.

In regard to α-amylase, it was not strongly inhibited by these substances. Similar results were obtained in the study of Yang et al. who proved, consistently with the previous report, that the inhibition of α-glucosidase by tea polyphenols is noncompetitive 13 , Furthermore, Gao et al.

also reported that the combination of acarbose and GTE, EGCG, or green tea polyphenols show combined inhibitory effects at certain concentrations Therefore, it could be expected that joined therapy with GTE or green tea polyphenols or EGCG may diminish the dose of acarbose needed in therapy, hence weaken the side effects of acarbose alone.

The aforesaid findings indicate that green tea or functional food based on green tea could be applicable for complementary therapy in postprandial hyperglycemia. We used naturally 13 C abundant cornflakes as a source of starch. The physical form of starch, the method of its processing or the size of the particle are a vital factors that may influence the hydrolysis and glycemic response in subjects Commercially available cereals used in the study, were produced via an extrusion process, which gives starch a high degree of gelatinization.

Based on the study of Hiele et al. starch in this formation is more rapidly hydrolysed than native starch Maize, a representative of C4 photosynthesizing plants incorporates more 13 C atoms into the starch than C3 plants do e.

European grain, potatoes, rice. The typical Polish diet in contrast to the American diet contains foodstuffs like potatoes, rye, wheat, beet sugar and to lesser extent maize, therefore maintaining the conditions of the test was easier.

Our data suggest that the use of GTE is a viable alternative to pharmaceutical inhibitors of glucoside hydrolase enzymes. This plant extract is widely available, inexpensive and well tolerated, so it has potential utility for weight control and the treatment of diabetes.

Our study supports the concept that pure GTE inhibits starch digestion and absorption. However, the clinical significance of each green tea catechin and the exact mechanism responsible for this action in humans remain to be determined. The study comprised of 28 healthy, adult volunteers 19 women and 9 men, aged 19—26 years old recruited from Vocational Technical High School for Computer Science in Nakło nad Notecią, Poland Table 3.

All subjects were recruited after they presented at an appointed meeting and showed willingness to participate the study, which was thereafter confirmed by informed written consent. The health status was defined as such: no physical complaints in the month preceding the study, no acute or chronic disease, no current pharmacotherapy, no past hospitalizations for gastroenterological indications and good nutritional status defined as weight, height and BMI within normal reference values.

As the subjects were to ingest milk, a hydrogen-methane breath test was performed in each subject, to exclude lactose malabsorption. In the first week of study, some of the participants ingested the test meal with GTE while the others ingested placebo.

The second test followed in a crossover manner. One week later, subjects who took GTE in the previous test were given placebo and those receiving placebo in the previous week were given GTE.

In this way subjects were internal self-controls to themselves. Exclusion criteria comprised: celiac disease, exocrine pancreatic insufficiency 32 , 33 and other gastrointestinal diseases, pharmacotherapeutics that might affect digestion and absorption of carbohydrates, antibiotic therapy within the preceding month and the use of beverages composed of green tea within the preceding month.

All subjects fasted for hours. The subjects were assigned to the groups randomly. One week later, the procedure was repeated, though the subjects ingested the opposite preparation from that ingested in the initial study. The subjects were also instructed to not eat any food with a naturally increased 13 C content, such as products made of maize, cane sugar, pineapple, kiwi fruit for 5 days preceding the examination.

The participants were asked not to consume any additional food or beverages and not to perform any physical activity in order to limit the glucose oxidation level and to only obtain the rate of starch hydrolysis. CPDR was considered to reflect digestion and absorption of dietary starch.

GTE was prepared according to the protocol described by Bajerska et al. Elena, Zelazkow, Poland. One gram of green tea aqueous extract dry matter contained 7. The study was carried out in accordance with the Declaration of Helsinki. Every subject provided written consent to participate after being informed about the aim and protocol of the research.

Results are expressed as medians and interquartile ranges. The statistical significance of differences between GTE and placebo tests was determined with the use of the Wilcoxon rank-sum test.

How to cite this article : Lochocka, K. et al. Green tea extract decreases starch digestion and absorption from a test meal in humans: a randomized, placebo-controlled crossover study.

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Feske S, Skolnik EY, Prakriya M. Ion channels and transporters in lymphocyte function and immunity. Fanger CM, Neben AL, Cahalan DM. Note: Content may be edited for style and length. Science News. Facebook Twitter Pinterest LinkedIN Email. FULL STORY.

RELATED TERMS Health benefits of tea White tea Oily fish Tea Gastrointestinal tract Ischaemic heart disease Calorie restricted diet Blood sugar.

Story Source: Materials provided by Ohio State University. Journal Reference : Joanna Hodges, Min Zeng, Sisi Cao, Avinash Pokala, Shahabbedin Rezaei, Geoffrey Sasaki, Yael Vodovotz, Richard Bruno.

Catechin-Rich Green Tea Extract Reduced Intestinal Inflammation and Fasting Glucose in Metabolic Syndrome and Healthy Adults: A Randomized, Controlled, Crossover Trial.

Cite This Page : MLA APA Chicago Ohio State University. ScienceDaily, 26 July Ohio State University. Green tea extract promotes gut health, lowers blood sugar. Retrieved February 13, from www. htm accessed February 13, Explore More. Fungi That Live in the Gut Influence Health and Disease.

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Green tea extract improves gut health, diminishes risks associated with metabolic syndrome EGCG and digestive health, the altered gut microbiota and its metabolites derived from EGCG intervention might djgestive a central role digesive these reversals. Considering Preventing premature aging potential interaction Ehalth gut microbiota and EGCG, we hypothesize that attenuation of EGCG and digestive health by EGCG ans mediated mainly through modulation digesitve the gut microbiota, which subsequently leads to alleviation of inflammation and oxidative stress in the host [ 1123 ]. In this mini review, we describe effects of green tea and the most important component EGCG in malignancy and inflammation. Oz HS, Chen T, de Villiers WJ. Sorry, a shareable link is not currently available for this article. According to the PCA biplot of the CON and UV groups, Clostridium butyricum was highly correlated with the UV group, and also significantly increased in the UV group compared to the CON.
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Health Conditions Discover Plan Connect. Type 2 Diabetes. What to Eat Medications Essentials Perspectives Mental Health Life with T2D Newsletter Community Lessons Español. Health News Fact Checked Green Tea Extract May Help Reduce Blood Sugar and Gut Inflammation.

By Meagan Drillinger on August 3, — Fact checked by Dana K. What the study found. What is metabolic syndrome? Green tea health risks. Staying healthy. How we reviewed this article: History. Aug 3, Written By Meagan Drillinger.

Share this article. Read this next. According to Nutritionists, These Are the 7 Ingredients Your Multivitamin Should Have. Medically reviewed by Lindsay Slowiczek, PharmD. By Arlene Semeco, MS, RD and Alyssa Northrop, MPH, RD, LMT. The 1-Hour Effects of Eating a Chocolate Chip Clif Bar.

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READ MORE. Type 2… READ MORE. Currently, Dr. Bruno and other researchers are looking at green tea and microbiota, a community of micro-organisms in the gut, to better understand whether green tea increases the levels of healthy bacteria while decreasing pathogenic populations of bacteria.

Green tea may benefit the heart, aid weight management, and soothe the skin. Learn more about the potential benefits and risks here. In this edition of Medical Myths, we tackle some persistent myths about supplements, including multivitamins, probiotics, and antioxidants.

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By Beth JoJack on August 1, — Fact checked by Patricia Weiser, PharmD. Forty participants -- 21 with metabolic syndrome and 19 healthy adults -- consumed gummy confections containing green tea extract rich in anti-inflammatory compounds called catechins for 28 days.

The daily dose equaled five cups of green tea. In the randomized double-blind crossover trial, all participants spent another 28 days taking a placebo, with a month off of any supplement between the treatments. Researchers confirmed that participants, as advised, followed a diet low in polyphenols -- naturally occurring antioxidants in fruits, vegetables, teas and spices -- during the placebo and green tea extract confection phases of the study so any results could be attributed to the effects of green tea alone.

Results showed that fasting blood glucose levels for all participants were significantly lower after taking green tea extract compared to levels after taking the placebo. Decreased gut inflammation due to the green tea treatment in all participants was established through an analysis that showed a reduction in pro-inflammatory proteins in fecal samples.

Using a technique to assess sugar ratios in urine samples, researchers also found that with green tea, participants' small intestine permeability favorably decreased.

Gut permeability, or leaky gut, enables intestinal bacteria and related toxic compounds to enter the bloodstream, stimulating low-grade chronic inflammation.

Bruno's lab is completing further analyses of microbial communities in the guts of study participants and levels of bacteria-related toxins in their blood. This work was supported by the U. Department of Agriculture and the Ohio Agricultural Research and Development Center at Ohio State.

Ohio State co-authors of both papers include Min Zeng, Geoffrey Sasaki, Sisi Cao, Yael Vodovotz and Joanna Hodges. Avinash Pokala and Shahabeddin Rezaei also co-authored the paper on glucose reduction.

Materials provided by Ohio State University. Original written by Emily Caldwell. Note: Content may be edited for style and length. Science News. Facebook Twitter Pinterest LinkedIN Email. FULL STORY. RELATED TERMS Health benefits of tea White tea Oily fish Tea Gastrointestinal tract Ischaemic heart disease Calorie restricted diet Blood sugar.

Story Source: Materials provided by Ohio State University. Journal Reference : Joanna Hodges, Min Zeng, Sisi Cao, Avinash Pokala, Shahabbedin Rezaei, Geoffrey Sasaki, Yael Vodovotz, Richard Bruno.

EGCG and digestive health -

Concentrations of myeloperoxidase MPO l , IL-6 m , and TNF-α n in the colon. To further assess the impact of EGCG on systemic and intestinal inflammatory response, myeloperoxidase MPO and pro-inflammatory cytokines in the plasma and colonic tissues were measured.

Plasma concentrations of IL-1β Fig. In contrast, rectal EGCG failed to suppress these cytokines in the plasma Additional file 1 : Figure S1h, Figure S1i, Figure S1j, and Figure S1k.

Similarly, DSS drastically elevated the concentration of MPO in the colon of mice, but such an elevation was significantly dampened by oral EGCG Fig. Furthermore, both oral and rectal EGCG significantly decreased the colonic levels of IL-6 Figs.

However, rectal EGCG failed to decrease the levels of MPO Additional file 1 : Figure S1l in the colon of DSS-treated mice.

Collectively, these results indicated that clinical colitis symptoms and colonic damage were ameliorated by oral, but not rectal, EGCG. To assess the influence of EGCG on oxidative stress, total antioxidant capacity T-AOC , total superoxide dismutases T-SOD , catalase CAT , glutathione peroxidase GSH-px , and malondialdehyde MDA in the plasma and colon were measured.

DSS-suppressed concentrations of T-SOD and CAT, and DSS-increased level of MDA in the plasma in the mice with colitis compared with normal controls were largely attenuated by oral EGCG Fig.

However, DSS-induced suppression of the plasma concentrations of T-SOD and CAT in the mice with colitis compared with normal controls were not obviously impacted by rectal EGCG, though the level of MDA was also decreased Additional file 2 : Figure S2a, Figure S2b, and Figure S2c.

The colonic levels of T-AOC and T-SOD were significantly decreased by DSS, but attenuated to normal by oral EGCG Fig. No significant differences in the levels of CAT or GSH-px Fig. Colonic concentration of MDA was attenuated to normal by oral EGCG Fig.

However, the effects of DSS on T-AOC, T-SOD, CAT, or MDA Additional file 2 : Figure S2d, Figure S2e, Figure S2f, and Figure S2h were not obviously impacted by rectal EGCG. Of note, GSH-px level in the colon was significantly increased by rectal EGCG even compared with the colon of the normal group Additional file 2 : Figure S2g.

However, both oral and rectal EGCG had no obvious effect on reducing apoptosis Figs. To assess the effect of oral or rectal EGCG on the colonic mucosal barrier, mucin-secreting goblet cells in the colonic epithelia were measured using Alcian blue staining.

DSS significantly reduced the thickness of colonic epithelial mucosa, and desirably, oral EGCG attenuated such damping to normal Fig. Consistently, oral EGCG largely reversed DSS-induced disruption in the fine structure of the brush border and tight junctions as revealed by transmission electron microscopy TEM Fig.

Oral EGCG attenuated oxidative stress and colonic damage. Concentrations of T-SOD a , CAT b , and MDA c in plasma from each group. d Level of T-AOC in the colon. j Representative fluorescent pictures of TUNEL staining of colonic sections.

Scale bars represent 50 μm. k Representative images of Alcian blue-stained inner mucus layer of colonic sections. l Representative images showing the microstructure of colonic epithelia by TEM. These results suggested that oral, but not rectal, EGCG suppressed DSS-induced oxidative stress, and attenuated DSS-damaged mucosal barrier function.

Next, we further explore the impact of EGCG on the gut microbiota composition of DSS-treated mice receiving oral or rectal EGCG via 16S rRNA gene sequencing. Alpha diversity shown by sobs index of ASV level was impacted by neither oral EGCG nor rectal EGCG in mice with colitis Fig.

Oral EGCG regulated the composition and function of intestinal microbiota. a α-diversity upon oral therapy represented by the Sobs index. b Principal coordinate analysis PCoA plots upon oral therapy assessed by PERMANOVA.

The relative abundance of fecal bacterial phyla c ; and genera d presented in e Analysis of differences in the microbial taxa shown by LEfSe linear discriminant analysis LDA coupled with effect size measurements upon oral therapy. Concentrations of fecal acetate f , propionate g , and butyrate h upon oral therapy.

i Spearman correlation between intestinal microbiota and anti-inflammatory or anti-oxidative parameters in DSS-treated mice in response to oral EGCG. The red color denotes a positive correlation, while blue color denotes a negative correlation.

The intensity of the color is proportional to the strength of Spearman correlation. At the phylum level, Bacteroidetes , Firmicutes , and Proteobacteria were predominant phyla in the fecal microbiota Fig.

Differentially abundant fecal bacterial taxa in DSS-treated mice in response to oral or rectal EGCG were identified by LEfSe analysis. Additionally, we found that four bacterial genera including Akkermansia were enriched by oral EGCG, while the other five taxa were enriched in the DSS only group Fig.

Two bacterial genera were particularly abundant in response to rectal EGCG, while other five taxa e. To further explore the effect of oral or rectal EGCG on the production of SCFAs, we measured the fecal concentrations of acetate, propionate, and butyrate.

All three SCFAs were significantly diminished by DSS, but the productions of propionate and butyrate were significantly improved by oral Fig. In fact, butyrate production was further significantly reduced in DSS-treated mice in response to rectal EGCG Additional file 3 : Figure S3h.

Spearman correlation analysis was further performed to understand the association between differentially enriched microbes and anti-oxidative, inflammatory parameters, or SCFAs profiles. Above all, alteration of the gut microbiota and increased production of SCFAs in mice with colitis occurred in response to oral, but not rectal EGCG administration, suggested that gut microbiota might play a critical role in alleviating DSS-induced colitis.

Given the benefit of green tea consumption in reducing the risk of IBD [ 13 ] and different impacts on the gut microbiota by oral and rectal delivery of EGCG, prophylactic effect of EGCG on DSS-induced colitis was then explored.

Mice were subjected to 2. Disease symptoms and body weight were monitored daily. Mice were then sacrificed and the colonic pathology was evaluated. The concentrations of several representative inflammatory mediators in both the plasma and the colon were also measured. Apparently, prophylactic EGCG alleviated the symptoms of colitis in DSS-treated mice as indicated by significantly reduced daily DAI Fig.

Histological analysis further revealed that prophylactic EGCG suppressed DSS-induced infiltration of inflammatory cells and damage to the colonic mucosa Fig. Moreover, prophylactic EGCG tended to reduce the plasma levels of IL-1β Fig.

Strikingly, DSS-elevated levels of MPO Fig. Prophylactic EGCG attenuated the symptoms of DSS-induced colitis. a Diagram illustrating the experimental design employed in this study. b Kinetics of DAI scores following DSS treatment. c Daily body weight changes following DSS treatment.

Concentrations of MPO l , IL-6 m , and TNF-α n in the colon. These results collectively indicated that prophylactic EGCG was capable of suppressing DSS-induced colitis symptoms, colonic injury, and inflammation.

Prophylactic EGCG largely attenuated the plasma levels of antioxidant enzymes, T-SOD, and CAT that were significantly reduced by DSS Fig. Consistently, MDA in the plasma was significantly increased by DSS, but reduced to normal in response to prophylactic EGCG Fig.

Similarly, the colonic levels of T-AOC Fig. The colonic level of MDA was significantly increased by DSS, but returned below normal in response to prophylactic EGCG Fig.

Of note, EGCG pre-supplementation even elicited an obvious anti-oxidative response in both the plasma and colon in healthy mice Fig. Prophylactic EGCG attenuated the oxidative stress and colonic damage. Concentrations of T-SOD a , CAT b , and MDA c in the plasma.

l Representative images for the microstructure of colonic epithelia by TEM. TUNEL analysis further revealed that DSS significantly increased the frequency of apoptotic cells in the colonic mucosa, but prophylactic EGCG largely reversed the trend Fig.

Moreover, prophylactic EGCG also attenuated the DSS-damaged colonic mucus and fine structure of colonic barrier Fig. These results suggested that prophylactic EGCG was capable of suppressing DSS-triggered oxidative stress, regulating apoptosis, and restoring mucosal barrier function in colonic epithelia.

Next, we investigated the impact of prophylactic EGCG on the gut microbiota composition of DSS-treated mice. Meanwhile, the overall fecal bacterial composition of mice at the phylum and genus level in all groups was consistent with the first trial Fig.

It was noteworthy that oral EGCG to healthy mice caused an enrichment of thirteen bacterial genera including Akkermansia while only four taxa were enriched in normal controls Fig.

Moreover, eight bacterial genera including Akkermansia , Faecalibaculum , and Bifidobacterium were enriched in mice with colitis treated by EGCG pre-supplementation, but another six genera were enriched in DSS-only group Fig. Additionally, prophylactic EGCG completely reversed the attenuation of SCFAs including acetate Fig.

Prophylactic EGCG regulated the composition and function of intestinal microbiota. a α-diversity represented by the Sobs index on day b PCoA plots on day 28 assessed by PERMANOVA among the four groups.

The relative abundance of fecal bacterial phyla c , and genera d presented in Analysis of differences in the microbial taxa between the CON group and EGCG group e , in DSS-treated mice with or without receiving EGCG f on day 27 was shown using LEfSe LDA coupled with effect size measurements.

Concentrations of fecal acetate g , propionate h , and butyrate i on day Spearman correlation between intestinal microbiota and anti-inflammatory or anti-oxidative parameters in healthy mice j , and in DSS-treated mice k in response to prophylactic EGCG.

Above all, these results indicated that prophylactic EGCG regulated the gut microbiota composition and its metabolism, leading to the potential to attenuate the DSS-induced dysbiosis. We next validated the impact of EGCG-mediated microbiota on murine colitis in the third animal trial via transplanting the fecal microbiota derived from mice receiving EGCG gavage to DSS-treated mice Fig.

As before, more increased body weight and colon length, and decreased DAI and histological damage was shown in mice with colitis treated by EGCG-FMT compared with other three groups Fig. As well, decreased levels of IL-1β, IL-6, IL-8, and TNF-α in the plasma Fig. Notably, it could not be neglected that EGCG-SFF also more profoundly alleviated the symptoms of acute colitis compared to mice with CON-SFF, indicated by less body weight loss, DAI score, and histological score, increased colonic length Fig.

Also, the plasma levels of IL-1β, IL-6, IL-8 Fig. EGCG-FMT alleviated DSS-induced experimental colitis better than CON-FMT and EGCG-SFF. EGCG-FMT and CON-FMT treatments were indicated.

b Kinetics of DAI scores throughout the entire duration of the study. d Macroscopic pictures of colons and f the lengths of colon from each group. Concentrations of MPO L , IL-6 M , and TNF-α N in the colon. Increased concentrations of T-SOD and CAT, and decreased concentration of MDA in the plasma of mice with colitis were observed by EGCG-FMT compared with other three groups Fig.

Also, increased concentrations of T-SOD and GSH-PX, and decreased concentration of MDA in the colon of mice with colitis were shown by EGCG-FMT compared with other three groups Fig.

Meanwhile, microbiota from EGCG-dosed mice promoted cell apoptosis and maintained better mucus distribution and integrity of tight junction in the colon in mice with colitis compared with CON-FMT or EGCG-SFF Fig. Notably, similar differences were shown in mice with EGCG-SFF compared to CON-SFF, indicated by increased plasma level of CAT, and colonic levels of T-SOD and GSH-PX, and decreased level of MDA in the plasma and colon Fig.

And the EGCG-SFF also promoted the apoptosis of colonic epithelium Fig. EGCG-FMT alleviated oxidative stress and colonic damage better than CON-FMT and EGCG-SFF.

Concentrations of T-SOD a , CAT b , and MDA c in the plasma from each group. The composition of gut microbiota upon FMT or SFF was also analyzed. Sobs index of ASV level was not significantly impacted by FMT or SFF in mice with colitis Fig. The main composition in both phylum and genus levels was similar among groups Fig.

Of note, the genus Akkermansia , was significantly enriched by EGCG-FMT Fig. Also, the productions of fecal SCFAs acetate, propionate, and butyrate in mice with colitis were significantly increased by EGCG-FMT than other three groups where the productions of SCFAs were not significantly impacted by EGCG-SFF compared to CON-SFF Fig.

EGCG-FMT promoted the enrichment of SCFAs-producing bacteria and production of SCFAs. b PCoA plots upon FMT or SFF assessed by PERMANOVA analysis. e Analysis of differences in the microbial taxa shown by LEfSe LDA coupled with effect size measurements upon FMT. Concentrations of fecal acetate f , propionate g , and butyrate h upon FMT.

i Spearman correlation between intestinal microbiota and anti-inflammatory or anti-oxidative parameters in DSS-treated mice in response to FMT or SFF.

Overall, EGCG-FMT alleviated colitis and colonic barrier damage in mice with colitis more profoundly than CON-FMT or EGCG-SFF. In agreement with our therapeutic and pre-supplemented trials, enriched Akkermansia and increased SCFAs production were also induced by EGCG-FMT, which indicated alleviated effects of gut microbiota from EGCG-dosed mice on colitis.

Besides host genetics, environmental factors such as dietary preference and gut microbiota have been associated with the development and progression of IBD [ 11 , 13 , 32 , 33 , 34 ]. Gut microbiota constitutes a critical bridge between environmental factors and host health, where the metabolites of microbiota such as SCFAs may exert anti-inflammatory function [ 35 , 36 , 37 ].

Daily consumption of tea has been shown to reduce the risk of IBD [ 12 , 13 ], and whether the protective effects of its functional components associate with gut microbiota has arisen the attention [ 38 , 39 ]. In agreement with our results between normal controls and mice with colitis, gut microbiota dysbiosis is the character of intestinal diseases, where the therapeutic strategies in modulating gut microbiota such as FMT have arisen the attention [ 40 , 41 ].

Here, we found that EGCG modulated gut microbiota composition and its metabolites, namely, enriching the SCFAs-producing bacteria such as Akkermansia , increasing the SCFAs production, and therefore promoting an anti-inflammatory and anti-oxidative state in the gut. Also, we demonstrate that gut microbiota and its metabolites induced by EGCG played a key role in the attenuation of DSS-induced experimental colitis, as supported by the more profoundly alleviated effects from EGCG-FMT than CON-FMT and EGCG-SFF.

To explore how oral or rectal EGCG attenuated the colitis, acute colitis of mice was induced by 2. In agreement with previous studies [ 16 , 17 ], we confirmed that the therapeutic applications of oral EGCG have led to the alleviation in DSS-induced colitis, as indicated by the decreased DAI and histological damage.

Consistent with previous studies [ 16 , 42 , 43 , 44 , 45 ], oral EGCG also alleviated colonic inflammation as exemplified by the decline of inflammatory cytokines such as IL-6 and TNF-α in both the plasma and colon of DSS-treated mice. Furthermore, we found that rectal delivery of EGCG failed to attenuate intestinal inflammation and pathology, which was supported by its little toxicity on rectal mucosa [ 46 ].

Moreover, therapeutic oral EGCG significantly attenuated DSS-induced oxidative stress by increasing the synthesis of antioxidant enzymes such as T-SOD and CAT, and decreasing the production of MDA in the colon and plasma.

In agreement with it, a previous study has revealed that therapeutic EGCG showed similar anti-oxidative effects [ 17 ]. Moreover, oral EGCG alleviated DSS-induced damage in integrity and barrier function as evidenced by the increased colonic mucus as well as the enhanced tight junctions and ultrastructure of the colonic mucosa in agreement with previous studies [ 47 , 48 , 49 , 50 ] while rectal EGCG did not.

Above all, different exposure of EGCG resulted in reversed effects, namely, oral EGCG alleviated colitis while rectal EGCG even exacerbated it. Considering that rectal EGCG has previously been demonstrated to impact the rectal infection of viruses [ 46 ], we hypothesized that those reversed results were due to their different impacts on gut microbiota and its metabolism.

Importantly, oral and rectal EGCG differentially impacted the gut microbiota and its metabolism. PCoA analyses revealed that gut microbiota structure was significantly impacted by oral EGCG and rectal EGCG, though community richness revealed by sobs index was not obviously impacted in mice with colitis by these two delivery routes.

As expected, therapeutic oral EGCG significantly increased SCFAs-producing bacteria including Akkermansia , and subsequently promoted the production of SCFAs. Moreover, the correlation analysis suggested that the relative abundance of Akkermansia was positively correlated with the SCFAs production, anti-oxidant enzymes, but negatively correlated with pro-inflammatory cytokines.

On the other hand, Akkermansia was not enriched by rectal EGCG. Similarly, previous studies have revealed that EGCG effectively reduced diet-increased obesity, and promoted the colonization of Akkermansia muciniphila , but how it impacted microbiota metabolites was unclear [ 38 , 51 ]. Also, a recent study has shown that the high fat diet-induced mRNA expression levels of pro-inflammatory cytokines IL-6, IL-1β were significantly reversed by Akkermansia muciniphila [ 52 ].

However, Lactobacillus levels and butyrate production in mice with colitis were further decreased by rectal EGCG compared to the group treated only with DSS. Lactobacillus , as the most common probiotics, is considered to exert extensive anti-inflammatory effects where lactate may play a role [ 53 ].

The decreased Lactobacillus levels and butyrate production have been demonstrated to induce the exacerbation of colitis in mice [ 11 ]. These outcomes indicated that the composition and metabolites of gut microbiota in mice with colitis were differentially modulated by the two exposure ways of EGCG.

Oral EGCG contributed to a stable microenvironment while rectal EGCG reversely. Also, the altered gut microbiota and its metabolites derived from EGCG intervention might play a central role in these reversals. Next, we further validated these probiotic effects by long-term administration of prophylactic EGCG, also as a simulation of about four to eight cups of tea per day for an adult [ 31 ].

The mechanism of this exposure route on attenuating the experimental colitis was also explored. As with therapeutic oral EGCG, prophylactic EGCG effectively attenuated the symptoms of colitis.

Prophylactic EGCG also declined the levels of pro-inflammatory cytokines and increased the anti-oxidative level in both the plasma and colon of DSS-treated mice. Furthermore, prophylactic EGCG was also capable of increasing the level of GSH-px in the colon which might promote the anti-oxidative state more profoundly.

Also, integrity and barrier function was protected from DSS-induced damage by prophylactic EGCG. Interestingly, prophylactic EGCG obviously decreased the pro-inflammatory state and promoted anti-oxidative state of intestine in healthy mice, indicating that consumption of EGCG had the potential to improve intestinal barrier.

The microbiota composition and its metabolites were also significantly modulated by prophylactic EGCG in both healthy mice and mice with colitis. Community richness was not obviously impacted in mice with colitis by prophylactic EGCG. Interestingly, we found that prophylactic EGCG significantly increased the community richness in healthy mice, suggesting the potentially beneficial effects of EGCG in gut microenvironment for animals or humans in the future.

Also, the structure of microbial community was significantly impacted by prophylactic EGCG in both healthy mice and mice with colitis, reminding us that the altered microbiota might play a vital role in alleviating the development of colitis.

Moreover, prophylactic EGCG significantly increased SCFAs-producing bacteria including Akkermansia , and subsequently promoted the production of SCFAs, which was in accordance with therapeutic oral EGCG.

Similarly, the SCFAs-producing bacteria Akkermansia positively correlated with SCFAs production and anti-oxidant enzymes, but negative correlated with pro-inflammatory cytokines of mice upon prophylactic EGCG. And potential probiotics Bifidobacterium and Faecalibaculum were also enriched in mice with colitis treated by prophylactic EGCG.

Previous researches showed that Akkermansia muciniphila could release two kinds of SCFAs acetate and propionate , and the cross-feeding between Akkermansia muciniphila and butyrate-producing bacteria promoted the butyrate production [ 54 ].

Also, this similar cross-feeding has been shown between Bifidobacterium and butyrate-producing bacteria [ 55 ]. The endogenous Faecalibaculum rodentium in the murine gut has been shown to promote intestinal tumorigenesis where SCFAs plays a vital role [ 56 ].

These results indicated that SCFAs-producing bacteria and subsequent production of SCFAs might play a role in the attenuation of colitis. We next sought to demonstrate the role of SCFAs-producing bacteria and subsequent production of SCFAs mediated by EGCG and verified whether the impacted gut microbiota and metabolites was the results or the reason of alleviated colitis.

The murine model with experimental colitis was induced, and FMT or SFF from normal controls or EGCG-dosed mice were performed. Interestingly, acute colitis was successfully alleviated by EGCG-FMT. In consistent with that of EGCG itself, EGCG-FMT alleviated symptoms of colitis profoundly better than CON-FMT, suggesting that EGCG-mediated gut microbiota plays a dominant role in alleviating the colitis.

Also, EGCG-SFF showed better alleviated symptoms than CON-SFF, suggesting the role of metabolites could not be neglected.

EGCG-FMT significantly attenuated DSS-induced inflammatory response and oxidative stress shown by similar performances with those of oral EGCG and prophylactic EGCG. Based on those results, we demonstrated that gut microbiota and its metabolites mediated by EGCG was the reason for the alleviated effects.

Combining the significant impacts of prophylactic EGCG on microbial community in healthy mice and the successfully alleviated effects from EGCG-FMT, we believed that EGCG facilitated the other microbes which were of low abundance in normal controls and hence ameliorates colitis.

We then explored the difference between EGCG-FMT and EGCG-SFF. FMT and SFF did not significantly impact the community richness. The structure of microbial community was significantly impacted by EGCG-FMT while EGCG-SFF did not, which might because of the sterility in SFF.

As expected, EGCG-FMT significantly increased SCFAs-producing bacteria such as Akkermansia , and subsequently promoted the production of SCFAs. Akkermansia has also shown a similar correlation with the inflammatory and oxidative indexes from oral therapy of EGCG and prophylactic EGCG.

These outcomes indicated that the alleviated effect of EGCG-FMT was similar with that of EGCG itself. Notably, EGCG-FMT significantly promoted the production of SCFAs while EGCG-SFF did not, indicating that the release of SCFAs depended on SCFAs-producing bacteria.

Based on our results and the previous studies, the SCFAs and SCFAs-producing microbes Akkermansia might also exert a beneficial role in the interplay between the gut microbiota and green tea polyphenols for the therapy or prevention of diseases [ 57 , 58 , 59 , 60 ].

Even though it has been previously shown that EGCG directly upregulate anti-oxidative function and impact cell proliferation in vitro [ 18 , 19 ].

We thought that these direct effects did not play a primary role in vivo, as indicated by our results that mice with colitis treated by rectal EGCG trended to exacerbate colitis. As the most abundant tea polyphenol in green tea, it was likely that the beneficial effects of EGCG were mediated through more than one mechanism [ 61 , 62 ].

Besides the functional SCFAs, previous studies have revealed that some phenolic metabolites from EGCG degradation may play a critical role, alongside other beneficial activities of EGCG, in reducing intestinal inflammatory diseases [ 63 , 64 ].

It cannot be denied that mice treated by oral EGCG or prophylactic EGCG benefited from not only gut microbiota and functional SCFAs but also other phenolic metabolites. Based on our results, we believe that these functional secondary metabolites of EGCG did not play a major role in the alleviated symptoms.

This is mainly due to the fact that the major phenolic metabolites of EGCG such as phenyl-γ-valerolactones are easily absorbed in the body after degradation of EGCG by intestinal bacteria and excreted via urine [ 14 , 63 ]. In addition, EGCG has been metabolized and absorbed in donors when we collected feces for FMT and SFF, indicating that the fecal concentrations of these metabolites were pretty low.

However, the functional SCFAs could be continuously produced by SCFAs-producing bacteria depending on basal carbon and nitrogen source. Probably due to this, EGCG-SFF has also showed anti-inflammatory and anti-oxidative effects compared to CON-SFF, which seemed to be similar to EGCG-FMT.

Moreover, EGCG-FMT alleviated the acute colitis better than CON-FMT and SFF, suggesting that EGCG-modulated gut microbiota played a vital role in alleviating colitis.

Furthermore, EGCG-FMT enriched the SCFAs-producing bacteria such as Akkermansia and further increased the fecal level of SCFAs compared with EGCG-SFF, indicating that EGCG-FMT exerted more beneficial effects in the colitis of mice.

Based on this, we believe that the anti-inflammatory and anti-oxidative effects of SCFA-producing bacteria enriched by EGCG were mainly mediated by functional SCFAs. In addition, the extra addition of gut microbiota further contributes to subsequent production of SCFAs than SFF.

Collectively, our results suggested that EGCG-mediated microbial community, especially the enrichment of Akkermansia played a key role in the alleviation of colitis, which could be the major driving force behind reversal outcomes between oral and rectal deliveries of EGCG.

These increased populations of SCFAs-producing microbes and their metabolites induced by EGCG delivery might also be involved in maintaining the homeostatic balance in the colon by improving the colonic epithelial integrity and mucosal immunity [ 65 , 66 ].

These results are summarized in Fig. Taken together, we concluded that SCFAs-producing bacteria induced by EGCG, especially such as Akkermansia , and subsequent production of protective SCFAs contributes to the anti-oxidative and anti-inflammatory state, and further protected from the damage in colon.

A schematic model showing the mechanism by which oral, but not rectal, delivery of EGCG alleviated DSS-induced colitis.

Intestinal microbiota, oxidative stress, inflammation, and barrier integrity are all affected. Oral EGCG induced an alteration in the gut microbiota to enrich probiotic bacteria such as Akkermansia , which subsequently led to an increased production of SCFAs such as butyrate, triggering a cascade of anti-oxidative, anti-inflammatory, and barrier-protective response.

Ultimately, intestinal epithelial homeostasis is attenuated and colitis was attenuated. In summary, oral, but not rectal, delivery of EGCG attenuates DSS-induced colitis, and their different impacts on the composition and metabolites of gut microbiota, implies a central role of gut microbiota in mediating the beneficial effects.

Given the alleviated effect of microbiota from EGCG-dosed mice, the beneficial role for alleviating IBD progress by EGCG was believed to be mediated mainly through the SCFAs-producing bacteria especially such as Akkermansia and subsequent production of functional SCFAs.

These changes in gut microbiota subsequently lead to increased production of protective SCFAs such as butyrate, which in turn triggers a pronounced anti-oxidative, anti-inflammatory, and barrier-enhancing program, resulting in the attenuation of intestinal inflammation and damage.

The proposed mechanisms are summarized in Fig. These findings provide novel insights into the EGCG-mediated alleviation of IBD and will facilitate the development of therapeutic and preventive strategies for IBD and other inflammatory disorders.

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The typical Polish diet in contrast to the American diet contains foodstuffs like potatoes, rye, wheat, beet sugar and to lesser extent maize, therefore maintaining the conditions of the test was easier. Our data suggest that the use of GTE is a viable alternative to pharmaceutical inhibitors of glucoside hydrolase enzymes.

This plant extract is widely available, inexpensive and well tolerated, so it has potential utility for weight control and the treatment of diabetes.

Our study supports the concept that pure GTE inhibits starch digestion and absorption. However, the clinical significance of each green tea catechin and the exact mechanism responsible for this action in humans remain to be determined.

The study comprised of 28 healthy, adult volunteers 19 women and 9 men, aged 19—26 years old recruited from Vocational Technical High School for Computer Science in Nakło nad Notecią, Poland Table 3.

All subjects were recruited after they presented at an appointed meeting and showed willingness to participate the study, which was thereafter confirmed by informed written consent. The health status was defined as such: no physical complaints in the month preceding the study, no acute or chronic disease, no current pharmacotherapy, no past hospitalizations for gastroenterological indications and good nutritional status defined as weight, height and BMI within normal reference values.

As the subjects were to ingest milk, a hydrogen-methane breath test was performed in each subject, to exclude lactose malabsorption. In the first week of study, some of the participants ingested the test meal with GTE while the others ingested placebo.

The second test followed in a crossover manner. One week later, subjects who took GTE in the previous test were given placebo and those receiving placebo in the previous week were given GTE.

In this way subjects were internal self-controls to themselves. Exclusion criteria comprised: celiac disease, exocrine pancreatic insufficiency 32 , 33 and other gastrointestinal diseases, pharmacotherapeutics that might affect digestion and absorption of carbohydrates, antibiotic therapy within the preceding month and the use of beverages composed of green tea within the preceding month.

All subjects fasted for hours. The subjects were assigned to the groups randomly. One week later, the procedure was repeated, though the subjects ingested the opposite preparation from that ingested in the initial study.

The subjects were also instructed to not eat any food with a naturally increased 13 C content, such as products made of maize, cane sugar, pineapple, kiwi fruit for 5 days preceding the examination. The participants were asked not to consume any additional food or beverages and not to perform any physical activity in order to limit the glucose oxidation level and to only obtain the rate of starch hydrolysis.

CPDR was considered to reflect digestion and absorption of dietary starch. GTE was prepared according to the protocol described by Bajerska et al. Elena, Zelazkow, Poland. One gram of green tea aqueous extract dry matter contained 7.

The study was carried out in accordance with the Declaration of Helsinki. Every subject provided written consent to participate after being informed about the aim and protocol of the research. Results are expressed as medians and interquartile ranges.

The statistical significance of differences between GTE and placebo tests was determined with the use of the Wilcoxon rank-sum test. How to cite this article : Lochocka, K.

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Green tea aqueous extract reduces visceral fat and decreases protein availability in rats fed with a high-fat diet. N 31, — Download references. Department of Pediatric Gastroenterology and Metabolic Diseases, Poznan University of Medical Sciences, Poznan, Poland.

Klaudia Lochocka, Aleksandra Glapa, Ewa Fidler-Witon, Jan K. Department of Human Nutrition and Hygiene, Poznan University of Life Sciences, Poznan, Poland. Department of Neonatology, Poznan University of Medical Sciences, Poznan, Poland.

You can also search for this author in PubMed Google Scholar. designed the experiment; K. and A. performed the research; K. and J. analyzed data; K. wrote the manuscript; J. provided revisions. All authors reviewed the manuscript. This work is licensed under a Creative Commons Attribution 4.

Reprints and permissions. Lochocka, K. Sci Rep 5 , Download citation. Received : 16 January Accepted : 22 May Published : 30 July Anyone you share the following link with will be able to read this content:.

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The benefits of hezlth green tea are widely known, but new research is diyestive EGCG and digestive health that consuming green tea extract Healthy cooking techniques also improve gut health. This is the first time that digestice study digrstive looked at the health risks linked to the condition known as metabolic syndrome, which affects about one third of Americans. The clinical trial was conducted as a follow-up to a study that associated lower obesity and fewer health risks in mice that consumed green tea supplements. They also noted improvements to gut health. The new study, published in Current Developments in Nutrition, delivered some unexpected findings. Green tea supplements can also lower blood sugar and decrease gut inflammation and permeability in healthy people. Microbiome volume 9EGCG and digestive health number: Cite this znd. Metrics EGC. Alteration of the gut microbiota may contribute to healhh development of inflammatory bowel disease IBD. Epigallocatechingallate EGCGa major bioactive constituent of green tea, is known to be beneficial in IBD alleviation. However, it is unclear whether the gut microbiota exerts an effect when EGCG attenuates IBD.

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