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PubMed2001

Inhibition by white tea of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-induced colonic aberrant crypts in the F344 rat.

There is growing interest in the potential health benefits of tea, including the anticarcinogenic properties. We report here that white tea, the least processed form of tea, is a potent inhibitor of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced colonic aberrant crypts in the rat. Male Fischer 344 rats were treated for 8 wk with white tea (2% wt/vol) or drinking water alone, and on alternating days in experimental Weeks 3 and 4 the animals were given PhIP (150 mg/kg body wt p.o.) or vehicle alone. At the end of the study there were 5.65 +/- 0.81 and 1.31 +/- 0.27 (SD) aberrant crypt foci per colon in groups given PhIP and PhIP + white tea, respectively (n = 12, P < 0.05). No changes were detected in N-acetyltransferase or arylsulfotransferase activities compared with controls, but there was marked induction of ethoxyresorufin O-deethylase, methoxyresorufin O-demethylase, and UDP-glucuronosyltransferase after treatment with white tea. Western blot revealed corresponding increases in cytochrome P-450 1A1 and 1A2 proteins. Enzyme assays and Western blot also revealed induction of glutathione S-transferase by white tea. There was less parent compound and 4'-hydroxy-PhIP but more PhIP-4'-O-glucuronide and PhIP-4'-O-sulfate in the urine from rats given PhIP + white tea than in urine from animals given carcinogen + drinking water. The results indicate that white tea inhibits PhIP-induced aberrant crypt foci by altering the expression of carcinogen-metabolizing enzymes, such that there is increased ring hydroxylation at the 4' position coupled with enhanced phase 2 conjugation.

Animals↗
PubMed1997

Cancer rates among drinkers of black tea.

Studies in experimental animals have shown that compounds in tea can inhibit the process of carcinogenesis, with the beneficial effects accruing to both green and black teas. Herein epidemiologic studies around the world are reviewed to assess the rates and risks of cancer among black tea drinkers. Ecologic data suggest at most a modest benefit on total cancer, as there is considerable international variation in black tea consumption but generally small differences in overall cancer rates. Cohort studies of tea drinkers and case control studies of specific cancers show mixed results. Consistent dose-related patterns have yet to emerge, although detailed data from these studies on cancer risks according to amount and duration of black tea intake are often limited. Several investigations point to the possibility of somewhat lowered risks of digestive tract cancers among tea drinkers, but the evidence is inconclusive. Further research, especially involving populations with wide ranges of tea consumption, is needed to clarify black tea's impact on cancer risk.

Cohort Studies↗
PubMed2001

Addition of milk does not affect the absorption of flavonols from tea in man.

Tea is a major source of flavonols, a subclass of antioxidant flavonoids present in plant foods which potentially are beneficial to human health. Milk added to tea, a frequent habit in the United Kingdom, could inhibit absorption of tea flavonoids, because proteins can bind flavonoids effectively. Eighteen healthy volunteers each consumed two out of four supplements during three days: black tea, black tea with milk, green tea and water. A cup of the supplement was consumed every 2 hours each day for a total of 8 cups a day. The supplements provided about 100 micromol quercetin glycosides and about 60 - 70 micromol kaempferol glycosides. Addition of milk to black tea (15 ml milk to 135 ml tea) did not change the area under the curve of the plasma concentration-time curve of quercetin or kaempferol. Plasma concentrations reached were about 50 nM quercetin and 30 - 45 nM kaempferol. We conclude that flavonols are absorbed from tea and that their bioavailability is not affected by addition of milk.

Animals↗
PubMed1998

Effect of black tea on azoxymethane-induced colon cancer.

Two sets of experiments on the role of tea in azoxymethane (AOM) induced colon cancer were performed. The first test involved male F344 rats given 1.25% solutions of black tea beginning at 5 weeks of age and ending at 51 days of age. At 6 and 7 weeks of age, they received 15 mg/kg AOM and were held for 50 weeks. Another group received the AOM dosage at 6 and 7 weeks and were placed on the tea solutions 2 days after the last AOM dosage, at 51 days of age, and held for the 50-week period. The end point was the occurrence and multiplicity of colon cancer, classified as in situ, exophytic, invasive and Peyer's patch carcinomas. Tea failed to affect the incidence and multiplicity of colon cancers when given during or after the AOM administration, but tea after AOM increased the multiplicity of exophytic carcinomas. In a second series of tests, solutions of 0.6, 1.25, 1.75 or 2.5% tea were given, beginning 1 week prior to the two AOM doses and extending for 42 weeks. Also, one group received 1.25% tea and 1.85% whole milk. The incidence of exophytic or invasive colon cancer and tumor multiplicity were similar in all treatment groups, although the incidence of exophytic neoplasms was higher with 2.5% tea. Thus, chronic administration failed to significantly change the incidence and multiplicity of the AOM-induced colon cancers. These findings are accounted for by the underlying mechanism, namely the fact that tea solutions do not alter the amount of cytochrome P-4502E1 required for the metabolic activation of AOM.

Animals↗
PubMed2001

Green tea suppresses lipopolysaccharide-induced liver injury in d-galactosamine-sensitized rats.

We conducted a series of in vivo experiments to clarify the hepatoprotective activity of green tea against lipopolysaccharide (LPS) + D-galactosamine (GalN)-induced liver injury and to elucidate the mechanism by which green tea exerts its effect in 7-wk-old male Wistar rats. Liver injury was assessed by plasma alanine aminotransferase and aspartate aminotransferase activities. Green tea extract significantly suppressed LPS + GalN-induced liver injury when added to the diet (30 or 35 g/kg) and fed to rats for 14 d or when force-fed alone (0.4-1.2 g/kg body) 1.5 h before the injection of drugs. Although all five of the fractions extracted from green tea extract with different organic solvents had significant suppressive effects, the caffeine-containing fraction exhibited the strongest effect, suggesting that the protective effect of green tea against LPS + GalN-induced liver injury is attributable mainly to caffeine. Authentic caffeine also significantly suppressed LPS + GalN-induced liver injury when added to the diet (2 g/kg) and fed to rats for 14 d. Dietary green tea suppressed LPS + GalN-induced apoptosis of liver cells, as assessed by DNA fragmentation. However, dietary green tea did not suppress LPS-induced enhancement of plasma concentration of tumor necrosis factor (TNF)-alpha, the cytokine that is thought to play a pivotal role in the pathogenesis of LPS-induced liver injury, although it significantly suppressed plasma concentrations of interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-10 and interferon (IFN)-gamma. TNF-alpha + GalN-induced liver injury and apoptosis were also suppressed by dietary green tea. In contrast, dietary caffeine significantly suppressed LPS-induced enhancement not only of plasma IL-1beta, IL-6, IL-10 and IFN-gamma concentrations, but also of TNF-alpha concentration. The results suggest that green tea might suppress LPS + GalN-induced liver injury mainly through the inhibition of TNF-alpha-induced apoptosis of hepatocytes, rather than through the suppression of TNF-alpha production, although the suppressed production of TNF-alpha may be associated with the hepatoprotective effect of caffeine.

Alanine Transaminase↗
PubMed2003

Molecular targets for green tea in prostate cancer prevention.

Prostate cancer (PCa) is the most frequently diagnosed malignancy and the second leading cause of cancer-related deaths in American males. For these reasons, it is necessary to intensify our efforts for better understanding and development of novel treatment and chemopreventive approaches for this disease. In recent years, green tea has gained considerable attention as an agent that could reduce the risk of several cancer types. The cancer-chemopreventive effects of green tea appear to be mediated by the polyphenolic constituents present therein. Based on geographical observations that suggest that the incidence of PCa is lower in Japanese and Chinese populations that consume green tea on a regular basis, we hypothesized that green tea and/or its constituents could be effective for chemoprevention of PCa. To investigate this hypothesis, we initiated a program for the chemoprevention of PCa by green tea. In cell-culture systems that employ human PCa cells DU145 (androgen insensitive) and LNCaP (androgen sensitive), we found that the major polyphenolic constituent (-)-epigallocatechin-3-gallate (EGCG) of green tea induces 1) apoptosis, 2) cell-growth inhibition, and 3) cyclin kinase inhibitor WAF-1/p21-mediated cell-cycle dysregulation. More recently, using a cDNA microarray, we found that EGCG treatment of LNCaP cells results in 1) induction of genes that functionally exhibit growth-inhibitory effects, and 2) repression of genes that belong to the G-protein signaling network. In animal studies that employ a transgenic adenocarcinoma of the mouse prostate (TRAMP), which is a model that mimics progressive forms of human prostatic disease, we observed that oral infusion of a polyphenolic fraction isolated from green tea (GTP) at a human achievable dose (equivalent to 6 cups of green tea/d) significantly inhibits PCa development and metastasis. We extended these studies and more recently observed increased expression of genes related to angiogenesis such as vascular endothelial growth factor (VEGF) and those related to metastasis such as matrix metalloproteinases (MMP)-2 and MMP-9 in prostate cancer of TRAMP mice. Oral feeding of GTP as the sole source of drinking fluid to TRAMP mice results in significant inhibition of VEGF, MMP-2 and MMP-9. These data suggest that there are multiple targets for PCa chemoprevention by green tea and highlight the need for further studies to identify novel pathways that may be modulated by green tea or its polyphenolic constituents that could be further exploited for prevention and/or treatment of PCa.

Animals↗
PubMed2005

Tea catechins with a galloyl moiety suppress postprandial hypertriacylglycerolemia by delaying lymphatic transport of dietary fat in rats.

Tea catechins, (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECG), and (-)-epigallocatechin gallate (EGCG), have been shown to be epimerized to (-)-catechin (C), (-)-gallocatechin (GC), (-)-catechin gallate (CG), and (-)-gallocatechin gallate (GCG), respectively, during heat treatment. In this study, we examined the effect of tea catechins rich in ECG and EGCG and heat-treated tea catechins rich in CG and GCG on postprandial hypertriacylglycerolemia in rats. Both tea catechins and heat-treated tea catechins suppressed postprandial hypertriacylglycerolemia. Lymphatic recovery of (14)C-trioleoylglycerol in rats cannulated in the thoracic duct was delayed by the administration of tea catechins and heat-treated tea catechins. Tea catechins and heat-treated tea catechins had the same effect on all variables tested. These catechin preparations dose-dependently inhibited the activity of pancreatic lipase in vitro. When purified catechins were used, only those with a galloyl moiety inhibited the activity of pancreatic lipase. These results suggest that catechins with a galloyl moiety suppress postprandial hypertriacylglycerolemia by slowing down triacylglycerol absorption through the inhibition of pancreatic lipase. Because postprandial hypertriacylglycerolemia is a risk factor for coronary heart disease, our results suggest that catechins with a galloyl moiety may prevent this disease.

Animals↗
PubMed2001

Tea flavonoids and cardiovascular health.

Tea is rich in antioxidant polyphenols (catechins, flavonols, theaflavins and thearubigins). Epidemiological evidence relating regular consumption of tea or related polyphenols to CHD is equivocal. Catechins are absorbed from tea, but low plasma concentrations are attained. The bioavailability of theaflavins and thearubigins is unknown. Tea does not reduce blood pressure or plasma lipids in well-controlled human trials. Tea polyphenols inhibit LDL lipid peroxidation in vitro, but the effect ex vivo is small. The plasma antioxidant potential increases after drinking green but not black tea. Tea consumption tended to reduce the development of aortic atherosclerosis in rabbits. Tea polyphenols exert marked effects on cells, and inhibit neutrophil migration and inflammatory responses, sometimes at low concentrations. These diverging results suggest potential beneficial effects, but emphasize the need for good human trials of tea using early markers of CHD before firm conclusions can be drawn.

Animals↗
PubMed1994

Effect of decaffeination of coffee or tea on gastro-oesophageal reflux.

BACKGROUND: Coffee and tea are believed to cause gastro-oesophageal reflux; however, the effects of these beverages and of their major component, caffeine, have not been quantified. The aim of this study was to evaluate gastro-oesophageal reflux induced by coffee and tea before and after a decaffeination process, and to compare it with water and water-containing caffeine. METHODS: Three-hour ambulatory pH-metry was performed on 16 healthy volunteers, who received 300 ml of (i) regular coffee, decaffeinated coffee or tap water (n = 16), (ii) normal tea, decaffeinated tea, tap water, or coffee adapted to normal tea in caffeine concentration (n = 6), and (iii) caffeine-free and caffeine-containing water (n = 8) together with a standardized breakfast. RESULTS: Regular coffee induced a significant (P < 0.05) gastro-oesophageal reflux compared with tap water and normal tea, which were not different from each other. Decaffeination of coffee significantly (P < 0.05) diminished gastro-oesophageal reflux, whereas decaffeination of tea or addition of caffeine to water had no effect. Coffee adapted to normal tea in caffeine concentration significantly (P < 0.05) increased gastro-oesophageal reflux. CONCLUSIONS: Coffee, in contrast to tea, increases gastro-oesophageal reflux, an effect that is less pronounced after decaffeination. Caffeine does not seem to be responsible for gastro-oesophageal reflux which must be attributed to other components of coffee.

Adult↗
PubMed2001

A new function of green tea: prevention of lifestyle-related diseases.

In the normal human life span, there occur lifestyle-related diseases that may be preventable with nontoxic agents. This paper deals with the preventive activity of green tea in some lifestyle-related diseases. Green tea is one of the most practical cancer preventives, as we have shown in various in vitro and in vivo experiments, along with epidemiological studies. Among various biological effects of green tea, we have focused on its inhibitory effect on TNF-alpha gene expression mediated through inhibition of NF-kappaB and AP-1 activation. Based on our recent results with TNF-alpha-deficient mice, TNF-alpha is an endogenous tumor promoter. TNF-alpha is also known to be a central mediator in chronic inflammatory diseases such as rheumatoid arthritis and multiple sclerosis. We therefore hypothesized that green tea might be a preventive agent for chronic inflammatory diseases. To test this hypothesis, TNF-alpha transgenic mice, which overexpress TNF-alpha only in the lungs, were examined. The TNF-alpha transgenic mouse is an animal model of human idiopathic pulmonary fibrosis which also frequently develops lung cancer. Expressions of TNF-alpha and IL-6 were inhibited in the lungs of these mice after treatment with green tea in drinking water for 4 months. In addition, judging from the results of a prospective cohort study in Saitama Prefecture, Japan, green tea helps to prevent cardiovascular disease. In this study, a decreased relative risk of death from cardiovascular disease was found for people consuming over 10 cups of green tea a day, and green tea also had life-prolonging effects on cumulative survival. These data suggest that green tea has preventive effects on both chronic inflammatory diseases and lifestyle-related diseases (including cardiovascular disease and cancer), resulting in prolongation of life span.

Animals↗
PubMed1992

[Antimicrobial and microbicidal activities of tea and catechins against Mycoplasma].

We examined tea extracts, (-) epigallocatechin gallate (EGCg) and theaflavin digallate (TF3) for their antimicrobial and microbicidal activities against Mycoplasma. Green tea and black tea showed antimicrobial activities against M. pneumoniae. At a concentration of 0.2% green tea and black tea showed microbicidal activities against M. pneumoniae and M. orale but not against M. salivarium. Extracts of pu-erh tea showed a slight microbicidal activity against M. pneumoniae and M. orale. EGCg purified from green tea and TF3 from black tea markedly showed microbicidal activities against M. pneumoniae. M. orale and M. salivarium. These results suggest that tea and catechins can be used as prophylactic agents against Mycoplasma pneumoniae infection.

Biflavonoids↗
PubMed2005

Addition of milk does not alter the antioxidant activity of black tea.

Tea is a polyphenol-rich beverage like wine and catechins are its chief polyphenols. Catechins have cardio-protective effects as they can scavenge free radicals and inhibit lipid peroxidation. Epidemiological studies indicate an inverse relation between tea consumption and the risk of cardiovascular and other chronic diseases. Addition of milk to black tea has been reported to adversely affect its beneficial effects, but the data are not unequivocal. Therefore, we assessed the effect of the addition of milk to black tea on its ability to modulate oxidative stress and antioxidant status in adult male human volunteers. Although the area under the curve of plasma catechins was lower on the consumption of tea with milk compared to black tea, it did not affect the beneficial effects of black tea on total plasma antioxidant activity, plasma resistance to oxidation induced ex vivo, and decreased plasma and urinary thiobarbituric acid reactive substance levels. The results suggest that addition of milk may not obviate the ability of black tea to modulate the antioxidant status of subjects and that consumption of black tea with/without milk prevents oxidative damage in vivo.

Adult↗
PubMedDate not supplied

Tea drinking and haemostasis: a randomized, placebo-controlled, crossover study in free-living subjects.

The hypothesis that tea drinking may protect against coronary heart disease (CHD) through effects on clotting as measured by plasma fibrinogen, tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) was tested in 65 healthy volunteers (31 men and 34 women; aged 20-74 years) in a randomized, blind, placebo-controlled, crossover study lasting 10 weeks (run-in phase 2 weeks, tea and placebo phases 4 weeks). During the placebo phase, intakes of milk, sugar, water and caffeine were matched to those in the tea phase during which 6 mugs of tea were drunk daily. Compliance with tea intake was measured by marking tea bags with p-aminobenzoic acid and measuring recovery in 24-hour urine collections. The mean +/- SD fibrinogen level, PAI-1 activity and tPA antigen level at baseline of 2.91 +/- 0.81 g/l, 7.9 +/- 5.3 U/ml and 4.76 +/- 2.17 ng/ml, respectively, were in the normal range. No significant differences in these variables between the run-in, tea or placebo phases were observed. The putative protective effect of tea against development of CHD is not mediated through effects of black tea on fibrinogen, tPA or PAI-1.

Adult↗
PubMed2004

Inhibition of lung carcinogenesis and effects on angiogenesis and apoptosis in A/J mice by oral administration of green tea.

Oral administration of tea (Camellia sinensis) has been shown to inhibit the formation and growth of several tumor types in animal models. The present study investigated the effects of treatment with different concentrations of green tea on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in female A/J mice. Two days after a single dose of NNK (100 mg/kg body weight, i.p.), the mice were given 0.1, 0.2, 0.4, and 0.6% green tea solution (1, 2, 4, and 6 g of tea solids, respectively, dissolved in 1 l of water), 0.02% caffeine, or water as the sole source of drinking fluid until the termination of the experiment. Only the treatment with 0.6% tea preparation significantly reduced lung tumor multiplicity (mean +/- SE, 6.07 +/- 0.77 vs. 8.60 +/- 0.50 tumors per mouse, P = 0.018). Treatment with 0.6% tea also inhibited angiogenesis, as indicated by the lower microvessel density (number of blood vessels/mm2) based on immunostaining for the von Willebrand factor antigen (81.9 +/- 9.5 vs. 129.4 +/- 8.2, P = 0.0018) and anti-CD31 antibody staining (465.3 +/- 61.4 vs. 657.1 +/- 43.6, P = 0.0012). Significantly lower vascular endothelial growth factor immunostaining scores were also observed in the 0.6% tea-treated group (0.98 +/- 0.17 vs. 1.43 +/- 0.07, P = 0.006). The apoptosis index was significantly higher in lung adenomas from 0.6% tea-treated mice based on morphological analysis of cell apoptosis (2.51 +/- 0.18% vs. 1.57 +/- 0.11%, P = 0.00005), and the result was further confirmed using the TUNEL method. Inhibition of angiogenesis and the induction of apoptosis by green tea may be closely related to the inhibition of pulmonary carcinogenesis.

Adenoma↗
PubMed2005

The effects of green tea ingestion over four weeks on atherosclerotic markers.

BACKGROUND: The objective of this study was to evaluate the effects of green tea ingestion over four weeks on atherosclerotic biological markers. METHODS: After a one-week baseline period, 12 healthy male volunteers aged 28--42 years drank 600 mL of green tea daily for four weeks. Lipid profile, oxidized low-density lipoprotein (ox-LDL), total antioxidant capacity (TAC), C-reactive protein (CRP) and soluble cell adhesion molecules were measured at baseline and after two and four weeks ingestion of green tea. RESULTS: There was no significant change in the concentrations of lipid profile, TAC, CRP, soluble intercellular adhesion molecule-1 (sICAM-1), or soluble E-selectin after ingestion of green tea. The levels of ox-LDL and soluble vascular cell adhesion molecule-1 (sVCAM-1) were significantly decreased after four weeks of green tea ingestion (Wilcoxon signed rank test, P=0.006). CONCLUSIONS: The results of this study suggest an in vivo anti-oxidative effect for green tea and an influence of green tea on atherosclerotic biological markers. The effect of green tea seen on ox-LDL and sVCAM-1 provides a potential mechanism for the cardiovascular benefits of regular ingestion of green tea.

Adult↗
PubMed1986

Protein conversion efficiencies of four test diets based on milk, two milk and tea treatments, and casein.

Milk consumption in 80 households in western Kenya averaged .25 to 1.00 L per family per day. Most of this milk was processed into a milk and tea beverage. Polyphenols, the major determinants of tea flavor and character, form soluble complexes with casein when black tea infusions are mixed with milk. Test diets were prepared from the following treatments: a) casein reference diet; b) milk, no tea leaves; c) milk added after heat treatment; and d) traditional Kenyan-style tea (i.e., milk and tea leaves heated together). Four groups of 10 male 21-day-old Sprague Dawley weanling rats were assembled and assigned to the test diets. Weight gain and protein intake (g/g) during a 28-d test period for the four diets were 1.94, 2.99, 2.93, and 2.77. The least significant difference test showed weight gain for protein intake was greater for rats on the milk-based diet and the diet with milk added after heating than for rats on the traditionally prepared milk and tea drink. Rats did most poorly when assigned to the casein reference diet. Modification of traditional Kenyan tea preparation practices (i.e., adding milk after tea leaves have been removed) might improve the nutritional value of the most popular milk product in western Kenya.

Animals↗
PubMed1986

Effect of green tea catechins on plasma cholesterol level in cholesterol-fed rats.

Effects of tea catechins (tannins) on lipid metabolism were studied in male weanling rats fed a 25% casein diet containing 15% lard and 1% cholesterol for 28 days. Crude tea catechins prepared from green tea powder were supplemented at a 1% and 2% of the lard-cholesterol diet. The addition of 2% tea catechins slightly depressed growth but at the 1% level was without effect. Tea catechins decreased plasma total cholesterol, cholesterol ester, total cholesterol--HDL-cholesterol (VIDL-+LDL-cholesterol) and atherogenic index (VLDL-+LDL-cholesterol/HDL-cholesterol). Hematocrit and plasma glucose were not altered by the addition of tea catechins. The liver weight, liver total lipids and cholesterol concentrations in rats fed the lard-cholesterol diet increased more than in the control rats, but the addition of tea catechins to the lard-cholesterol diet decreased those parameters. Tea catechin supplementation increased fecal excretion of total lipids and cholesterol. The results demonstrate that tea catechins exert a hypocholesterolemic effect in cholesterol-fed rats.

Animals↗
PubMed2005

Randomized controlled trial for an effect of green tea consumption on insulin resistance and inflammation markers.

To study the effects of the intake of green tea and polyphenols, which are a component of green tea, on insulin resistance and systemic inflammation, a randomized controlled trial was conducted on 66 patients aged 32-73 y (53 males and 13 females) with borderline diabetes or diabetes. Subjects in the intervention group were asked to take a packet of green tea extracts/powder containing 544 mg polyphenols (456 mg catechins) daily, which was a dose that could be taken without difficulty, and were asked to divide the green tea extracts/powder in a packet into 3 or 4 fractions dissolved in hot water everyday and to take a fraction after every meal or snack for 2 mo, in addition to daily food intake. The subjects in the control group were simply followed. To calculate the level of green tea polyphenol intake that the subject usually drank at home, the subject was asked to taste 3 teas of different strengths (1, 2 and 3%) and the tea that was closest to the one that the subject drank at home, was selected by each subject. After 2 mo, the mean daily polyphenol intake in the intervention group was 747 mg, which was significantly higher than that of 469 mg in the control group. In the intervention group, the body weight, BMI, systolic and diastolic blood pressures, blood glucose level, Hb A1c level, insulin level and HOMA index after taking the supplementation for 2 mo, were lower than the respective value before intervention: however, these parameters in the intervention group at 2 mo did not significantly differ from those in the control group. Within the intervention group, changes in insulin level tended to be associated with changes in polyphenol intake. In addition, changes in BMI were associated with changes in blood glucose level and insulin level. In conclusion, the daily supplementary intake of 500 mg green tea polyphenols did not have clear effects on blood glucose level, Hb A1c level, insulin resistance or inflammation markers. The positive correlation between the level of polyphenol intake and insulin level warrants further studies on the effect of green tea on insulin resistance.

Adult↗