Modulation of endocrine systems and food intake by green tea epigallocatechin gallate

Green tea polyphenols, especially the catechin, (-)-epigallocatechin gallate (EGCG), have been proposed as a cancer chemopreventative based on a variety of laboratory studies. For clear assessment of the possible physiological effects of green tea consumption, we injected pure green tea catechins ip into rats and studied their acute effects on endocrine systems. We found that EGCG, but not related catechins, significantly reduced food intake; body weight; blood levels of testosterone, estradiol, leptin, insulin, insulin-like growth factor I, LH, glucose, cholesterol, and triglyceride; as well as growth of the prostate, uterus, and ovary. Similar effects were observed in lean and obese male Zucker rats, suggesting that the effect of EGCG was independent of an intact leptin receptor. EGCG may interact specifically with a component of a leptin-independent appetite control pathway. Endocrine changes induced by parenteral administration of EGCG may relate to the observed growth inhibition and regression of human prostate and breast tumors in athymic mice treated with EGCG as well as play a role in the mechanism by which EGCG inhibits cancer initiation and promotion in various animal models of cancer.     

Epigallocatechin‐gallate modulates chemotherapy‐induced apoptosis in human cholangiocarcinoma cells

Background: Green tea polyphenols are chemopreventive in several cancer models but their use as adjunctive therapeutic agents for cancer is unknown. Aims: Cholangiocarcinomas respond poorly to chemotherapeutic agents and our aims were to assess the utility of green tea polyphenols as adjuncts to chemotherapy for cholangiocarcinoma. Materials and Methods: We assessed the effect of purified green tea catechins on chemotherapy‐induced apoptosis in KMCH, CC‐LP‐1 and Mz‐ChA‐1 human cholangiocarcinoma cells, and on chemosensitivity of Mz‐ChA‐1 cell xenografts in nude mice. Results: Epigallocatechin‐gallate (EGCG), but not the structurally related catechin epigallocatechin, sensitized cells to apoptosis induced by gemcitabine (GEM), mitomycin C or 5‐fluorouracil in vitro. Mitochondrial membrane depolarization, cytosolic cytochrome c expression and apoptosis were increased in cells incubated with EGCG and GEM compared with either agent alone. Furthermore, EGCG decreased in vivo growth and increased the sensitivity to GEM of Mz‐ChA‐1 cell xenografts in nude mice. Conclusions: The green tea polyphenol EGCG sensitizes human cholangiocarcinoma cells to chemotherapy‐induced apoptosis and warrants evaluation as an adjunct to chemotherapy for the treatment of human cholangiocarcinoma.     

Catechin-vanilloid synergies with potential clinical applications in cancer

A cancer-specific cell surface protein, tNOX, has been identified as a target for low-dose cell killing (apoptosis) of cancer cells by green tea catechins and Capsicum vanilloid combinations. This protein is uniquely associated with all forms of cancer and is absent from normal cells and tissues. Its activity is correlated with cancer growth. When blocked, cancer cells fail to enlarge after division and eventually die. Among the most potent and effective inhibitors of tNOX are naturally occurring polyphenols exemplified by the principal green tea catechin (-)-epigallocatechin gallate (EGCg) and the vanilloid capsaicin. Catechin-vanilloid combinations are 10 to 100 times more effective than either catechins or vanilloids alone. Vector-forced overexpression of tNOX cDNA and antisense has demonstrated that the tNOX target is both necessary and sufficient to explain the anticancer properties of green tea catechins alone and in vanilloid-containing combinations. The necessity and sufficiency of tNOX was validated as the catechin target with transgenic mice overexpressing the processed form of tNOX. Transgenic mice grew faster and the increased growth caused by tNOX overexpression was blocked by EGCg in the drinking water. A catechin-vanilloid mixture where one 350-mg capsule is equivalent to 16 cups of green tea in its ability to inhibit tNOX and growth of cancer cells in culture is undergoing clinical evaluation as a therapeutic aid for cancer patients.     

Matrix metalloproteinase-9 overexpression enhances vascular smooth muscle cell migration and alters remodeling in the injured rat carotid artery

Matrix metalloproteinase-9 (MMP-9) has been implicated in the pathogenesis of atherosclerosis as well as intimal hyperplasia after vascular injury. We used Fischer rat smooth muscle cells (SMCs) overexpressing MMP-9 to determine the role of MMP-9 in migration and proliferation as well as in vessel remodeling after balloon denudation. Fischer rat SMCs were stably transfected with a cDNA for rat MMP-9 under the control of a tetracycline-regulatable promoter. In this system, MMP-9 was overexpressed in the absence, but not in the presence, of tetracycline. In vitro SMC migration was determined using a collagen invasion assay as well as a Boyden chamber assay. In vivo migration was determined by measuring the invasion into the medial and intimal layers of transduced SMCs seeded on the outside of the artery. Transduced SMCs were also seeded on the luminal surface, and the effect of local MMP-9 overexpression on vascular structure was measured morphometrically at intervals up to 28 days. MMP-9 overexpression enhanced SMC migration in both the collagen invasion assay and Boyden chamber in vitro, increased SMC migration into an arterial matrix in vivo, and altered vessel remodeling by increasing the vessel circumference, thinning the vessel wall and decreasing intimal matrix content. These results demonstrate that MMP-9 enhances vascular SMC migration in vitro and in vivo and alters postinjury vascular remodeling.     

Catechins prevent vascular smooth muscle cell invasion by inhibiting MT1-MMP activity and MMP-2 expression

OBJECTIVE: Regular consumption of green tea is associated with a reduced risk of mortality due to coronary diseases and cancer. The present study examined whether a green tea extract (GTE) inhibits activation of matrix metalloproteinase-2 (MMP-2), a major collagenase involved in vascular remodeling of atherosclerotic plaques, in vascular smooth muscle cells (VSMCs). METHODS AND RESULTS: The expression of MMP-2 was assessed by Northern and Western blot analyses in human aortic VSMCs. MMP-2 activity was evaluated by zymography, membrane-type1-MMP (MT1-MMP, MMP-14) activity by an enzymatic assay, and cell invasion by a modified Boyden chamber assay. The thrombin-induced activation of secreted MMP-2 was abolished by GTE and the green tea polyphenols (-)-epigallocatechin-3-gallate (EGCG) and (-)-epicatechin-3-gallate (ECG). GTE reduced the expression of MMP-2 mRNA and protein. GTE, EGCG and ECG directly inhibited cell-associated MT1-MMP activity, the physiological activator of MMP-2, in a reversible manner. Thrombin-stimulated VSMCs invasion was abolished by EGCG and ECG, and reduced by GTE. CONCLUSIONS: GTE inhibits thrombin-induced VSMCs invasion most likely by preventing MMP-2 expression and its activation by a direct inhibition of MT1-MMP. The ability of green tea to prevent cell invasion and matrix degradation might contribute to its protective effect on atherosclerosis and cancer.     

eNOS gene transfer inhibits smooth muscle cell migration and MMP-2 and MMP-9 activity

Vascular smooth muscle cell (SMC) migration is a critical step in the development of neointima after angioplasty. Matrix metalloproteinases (MMPs) degrade the basement membrane and the extracellular matrix, facilitating SMC migration. Transfer of the endothelial nitric oxide synthase (eNOS) gene to the injury site inhibits neointima formation. Neither the signaling pathways leading to NO-mediated inhibition of SMC migration and proliferation nor the alterations in these pathways have been characterized. We hypothesize that NO inhibits SMC migration in part by regulating MMP activity. To test this hypothesis, we transfected cultured rat aortic SMCs with replication-deficient adenovirus containing bovine eNOS gene and analyzed the conditioned medium for MMP activity. We observed that eNOS gene transfer significantly (P<0.05) inhibited SMC migration and significantly (P<0.05) decreased MMP-2 and MMP-9 activities in the conditioned medium. Similarly, addition of the NO donor DETA NONOate and 8-bromo-cGMP to the culture medium significantly decreased MMP-2 and MMP-9 activities in the conditioned medium collected 24 hours after treatment. Furthermore, Western blot analysis of the conditioned medium collected from eNOS gene-transfected SMCs showed a significant increase in tissue inhibitor of metalloproteinases-2 (TIMP-2) levels. Our data suggest that NO decreases MMP-2 and MMP-9 activities and increases TIMP-2 secretion, and this shifts the balance of MMP activity, which may favor the inhibition of cell migration because of inhibition of extracellular matrix degradation.     

Factor Xa releases matrix metalloproteinase-2 (MMP-2) from human vascular smooth muscle cells and stimulates the conversion of pro-MMP-2 to MMP-2: role of MMP-2 in factor Xa-induced DNA synthesis and matrix invasion

Pro-matrix metalloproteinase-2 (pro-MMP-2) is expressed in vascular smooth muscle cells (SMCs). We report that activated coagulation factor X (FXa) induces the release of MMP-2 (65 kDa) from human SMCs. In addition, FXa cleaves pro-MMP-2 (72 kDa) into MMP-2. Pro-MMP-2 and MMP-2 were determined by gelatin zymography. MMP-2 was generated in conditioned medium containing pro-MMP-2 in a concentration-dependent fashion by FXa (3 to 100 nmol/L). FX at concentrations up to 300 nmol/L was ineffective. The conversion of pro-MMP-2 to MMP-2 was inhibited by a selective FXa inhibitor (DX-9065a) at 3 to 10 micromol/L. There was a concentration-dependent induction of an intermediate MMP-2 form (68 kDa) in lysates of FXa-treated cells. This indicates that cellular mechanisms are involved in FXa-induced conversion of pro-MMP-2. As a possible biological consequence of MMP-2 activation by FXa, DNA synthesis and matrix invasion of SMCs were determined. Both were stimulated by FXa and inhibited by the selective FXa inhibitor DX-9065a and the MMP inhibitor GM 6001 but not by hirudin or aprotinin. It is concluded that stimulation of SMCs by FXa increases the levels of MMP-2 in the extracellular space and that two different mechanisms are involved: release of active MMP-2 and cleavage of secreted pro-MMP-2. Both might contribute to the mitogenic potency of FXa and FXa-stimulated matrix invasion of SMCs.     

Epigallocatechin Gallate (EGCG), a Green Tea Polyphenol,Reduces Coronavirus Replication in a Mouse Model

The COVID-19 pandemic has resulted in a huge number of deaths from 2020 to 2021; however, effective antiviral drugs against SARS-CoV-2 are currently under development. Recent studies have demonstrated that green tea polyphenols, particularly EGCG, inhibit coronavirus enzymes as well as coronavirus replication in vitro. Herein, we examined the inhibitory effect of green tea polyphenols on coronavirus replication in a mouse model. We used epigallocatechin gallate (EGCG) and green tea polyphenols containing more than 60% catechin (GTP60) and human coronavirus OC43 (HCoV-OC43) as a surrogate for SARS-CoV-2. Scanning electron microscopy analysis results showed that HCoV-OC43 infection resulted in virion particle production in infected cells. EGCG and GTP60 treatment reduced coronavirus protein and virus production in the cells. Finally, EGCG- and GTP60-fed mice exhibited reduced levels of coronavirus RNA in mouse lungs. These results demonstrate that green tea polyphenol treatment is effective in decreasing the level of coronavirus in vivo.     

Preventive and therapeutic effects of green tea on lung cancer: a narrative review of evidence from clinical and basic research

Background and ObjectiveGreen tea is a popular beverage worldwide and has numerous health-promoting properties. Accumulating evidence indicates that green tea has preventive and therapeutic effects on lung cancer. This study aimed to investigate the association between green tea consumption and lung cancer.MethodsWe performed a narrative review to summarized the association between green tea consumption and lung cancer.Key Content and FindingsGreen tea consumption is known to decrease lung cancer risk in the general population, as indicated by meta-analyses of observational studies. Two active components of green tea, theabrownin and (−)-epigallocatechin gallate (EGCG), mediate the antitumor activity of green tea. Theabrownin promotes apoptosis, induces cell cycle arrest, and inhibits the migration, clone formation, and proliferation of lung cancer cell lines in vitro and in vivo. EGCG inhibits lung cancer cell proliferation and promotes apoptosis, agenesis, and epithelial-mesenchymal transition (EMT). In addition, EGCG sensitizes lung cancer cells to cisplatin and tyrosine kinase inhibitors (TKIs). The possible molecular mechanisms underlying the antitumor activity of EGCG and theabrownin were reviewed.ConclusionsObservational studies have indicated that green tea has preventive effects on lung cancer. In vitro and animal studies have indicated that green tea has therapeutic effects on lung cancer. Further clinical trials are needed to illustrate the therapeutic effects of green tea or its active components (i.e., theabrownin, EGCG) on lung cancer.     

Platelet aggregation induced by the C-terminal peptide of thrombospondin-1 (4N1-1) is inhibited by epigallocatechin gallate but not by prostaglandin E1

The C-terminal peptide of thrombospondin (4N1-1) stimulates distinct signalling pathways but induces an activation-independent platelet aggregation. This study demonstrates inhibitory effects of epigallocatechin gallate (EGCG), a major flavonoid component of green tea, on 4N1-1-induced aggregation of washed human platelets. Thrombin (0.1 U/ml)-induced platelet aggregation was completely inhibited by prostaglandin E1 (PGE1, 300 nM). In contrast, platelet aggregation induced by 4N1-1 (100 microM) was not affected by PGE1. However, epigallocatechin gallate (EGCG), but not other catechins from green tea, concentration-dependently inhibited 4N1-1-induced platelet aggregation. Thus, dietary components, such as EGCG, may inhibit platelet function even under conditions, when 'classical' platelet inhibitors, such as cAMP-elevating agents, are not effective.     

表没食子儿茶素没食子酸酯抗肿瘤侵袭转移相关机制的探讨

目的观察茶多酚的有效成分表没食子儿茶素没食子酸酯（EGCG）对人肝癌细胞侵袭转移的影响及探讨其相关机制。方法用免疫细胞化学检测黏蛋白1的表达、人工重组基底膜侵袭小室及明胶酶谱法观察其对人肝癌细胞株HepG2细胞侵袭转移的影响。结果EGCG能抑制HepG2细胞黏蛋白1的表达，对照组HepG2强阳性细胞数为15个，而EGCG组的强阳性细胞数为1个，差异有统计学意义；EGCG能抑制侵袭基底膜的能力，对照组的侵袭细胞数为（53．2±12．6）个，而EGCG组侵袭细胞数为（8．0±5．1）个，差异有统计学意义。EGCG能抑制MMP-2、MMP-9的分泌。结论EGCG具有明显的抗癌侵袭和转移的作用，其机制可能与黏蛋白1的降低有关。     

The protective effect of catechin on gastric mucosal lesions in rats,and its hormonal mechanisms

Background. Catechin, a polyphenol contained in tea (a cup of tea contains approximately 0.1% [w/v] catechin), has various physiological effects. The aim of this study was to investigate the mechanism of the inhibitory effect of catechin on gastric mucosal lesions. Methods. We studied the effect of catechin on gastric mucosal lesions in rats, using a water immersion restraint (WIR) stress-induced gastric mucosal lesion model. We used crude catechin that contained 52.6% (w/w) (−)-epigallocatechin gallate and 16.7% (w/w) (−)-epicatechin gallate. The rats were randomly divided into three groups; control rats freely drank distilled water, and the remaining rats drank 0.1% (w/v) or 1% (w/v) crude catechin-containing water for 2 weeks. We measured fractional areas of hemorrhagic erosion in the gastric mucosa induced by WIR stress for 4 h, compared with findings in the controls. We also employed an isolated rat stomach infusion model and measured gastrin, somatostatin, and histamine in the perfusate to endocrinologically investigate the mechanism underlying the putative protective effect of catechin. Results. Catechin had a significant protective effect against the gastric mucosal lesions induced by WIR stress. Catechin also significantly inhibited the release of gastrin, somatostatin, and histamine. Conclusions. Catechin confers a protective effect against gastric mucosal lesions, and anti-gastric and anti-histaminergic effects may be involved in the mechanism of this effect. Received: January 19, 2001 / Accepted: July 20, 2001     

All teas are not created equal: the Chinese green tea and cardiovascular health

Tea is one of the most widely consumed beverages in the world, next only to water. It can be categorized into three types, depending on the level of fermentation, i.e., green (unfermented), oolong (partially fermented) and black (fermented) tea. In general, green tea has been found to be superior to black tea in terms of antioxidant activity owing to the higher content of (-)-epigallocatechin gallate. The processes used in the manufacture of black tea are known to decrease levels of the monometric catechins to a much greater extent than the less severe conditions applied to other teas. The cardioprotective effect of flavonoids from green tea can be attributed to not only antioxidant, antithrombogenic and anti-inflammatory properties but also improvement of coronary flow velocity reserve. In this article, I will discuss the effects of green tea on atherosclerosis, coronary heart disease, hypertension, diabetes, metabolic syndrome and obesity, and, finally, its comparison with black tea.     

Smooth muscle cell matrix metalloproteinase production is stimulated via alpha(v)beta(3) integrin

This study tests the hypothesis that alpha(v)beta(3) integrin receptors play a critical role in smooth muscle cell (SMC) migration after arterial injury and facilitate migration through the upregulation of matrix metalloproteinase (MMP) activity. We showed that beta(3) integrin mRNA was upregulated by SMCs in the balloon-injured rat carotid artery in coincidence with MMP-1 expression and early SMC migration. Treatment with the beta(3) integrin-blocking antibody F11 significantly decreased SMC migration into the intima at 4 days after injury, from 110.8+/-30.8 cells/mm(2) in control rats to 10.29+/-7.03 cells/mm(2) in F11-treated rats (P=0.008). By contrast, there was no effect on medial SMC proliferation or on medial SMC number in the carotid artery at 4 days. In vitro, we found that human newborn SMCs produced MMP-1 but that adult SMCs did not. This was possibly due to the fact that newborn SMCs expressed alpha(v)beta(3) integrin receptors, whereas adult SMCs did not. Stimulation of newborn (alpha(v)beta(3)+) SMCs with osteopontin, a matrix ligand for alpha(v)beta(3), increased MMP-1 production from 114.4+/-35.8 ng/mL at 0 nmol/L osteopontin to 232.5+/-57.5 ng/mL at 100 nmol/L osteopontin. Finally, we showed that stimulation of newborn SMCs with platelet-derived growth factor-BB and osteopontin together increased the SMC production of MMP-9. Thus, our results support the hypothesis that SMC alpha(v)beta(3) integrin receptors play an important role in regulating migration by stimulating SMC MMP production.     

Increased secretion of basement membrane-degrading metalloproteinases in pig saphenous vein into carotid artery interposition grafts.

Late saphenous vein bypass graft failure in humans involves medial and neointimal thickening as the result of migration and proliferation of vascular smooth muscle cells (SMCs). Recent work on angioplasty indicates that basement membrane-degrading metalloproteinases (MMPs) cooperate with growth factors to mediate SMC migration and proliferation. We sought evidence here for a similar role in experimental vein grafts in pigs. Tissue levels and secretion of MMP-2 and MMP-9 were compared by quantitative zymography in veins and grafts removed 2 to 168 days after implantation. Pro and active forms of MMP-2 were present in veins, but levels were increased in vein grafts after 7 days (4- and 6-fold, respectively) and 28 days (3-fold for both), returning to values in veins after 168 days. MMP-9 was not detected in veins, was increased in grafts after 2 days, further increased after 7 days (6-fold) and 28 days (15-fold), and declined to undetectable levels by 168 days. Immunocytochemistry detected increased expression of MMP-2 and MMP-9 with the same time course. MMP-2 was widely distributed, whereas MMP-9 was concentrated in highly proliferative SMCs at the superficial layers of the thickened neointima. We conclude that increased production of the basement membrane-degrading MMP-2 and MMP-9 spanned the period of neointima formation and SMC proliferation in experimental vein grafts. MMPs therefore constitute new therapeutic targets for reducing late vein graft failure.     

Matrix metalloproteinase and alphavbeta3 integrin-dependent vascular smooth muscle cell invasion through a type I collagen lattice

Smooth muscle cell (SMC) migration from the tunica media to the intima is a key event in the development of atherosclerotic lesions and in restenosis after angioplasty. SMCs require not only migratory but also degradative abilities that enable them to migrate through extracellular matrix proteins, which surround and embed these cells. We used a collagen type I lattice as a coating on top of a porous filter as a matrix barrier in a chamber to test the invasive behavior of SMCs in response to a chemoattractant (invasion assay) and compared that behavior with simple SMC migration through collagen type I-coated filters (migration assay). Inhibitors of matrix metalloproteinase, KB-R8301, tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), TIMP-2, and peptide 74, attenuated platelet-derived growth factor-BB (PDGF-BB)-directed SMC invasion across the collagen lattice, whereas no effect was seen with these inhibitors on simple SMC migration through collagen-coated filters. RGD peptide inhibited SMC invasion but did not affect SMC migration. Anti-alphavbeta3 integrin antibody attenuated PDGF-BB-directed SMC invasion, whereas other antibodies against RGD-recognizing integrins, namely alphavbeta5 and alpha5, had no effect. None of these antibodies had any effect on simple SMC migration. RGD peptide and anti-alphavbeta3 antibody inhibited the attachment and spreading of SMCs on denatured collagen but not on native collagen. These findings indicate that there is a difference in the mechanisms between simple SMC migration across a collagen-coated filter and SMC invasion through a fibrillar collagen barrier. A proteolytic process is required for SMC invasion, and the degradation of matrix proteins alters the relationship between matrix protein molecules and SMC surface integrins.     

Green tea catechins inhibit neointimal hyperplasia in a rat carotid arterial injury model by TIMP-2 overexpression

OBJECTIVE: Although it has been demonstrated that the antioxidant properties of tea catechins reduce atherosclerotic lesions in various animal models of hyperlipidemia, it is not yet clear whether these catechins prevent hyperlipidemia-independent arterial remodeling induced by balloon angioplasty. We evaluated the influence of the administration of the tea extract on vascular remodeling in a rat carotid artery balloon-injury model. METHODS AND RESULTS: Male Wistar rats were supplied drinking water with or without green tea extract (1 mg/ml) supplement. Administration of the tea extract reduced the area of the intima (30%) and the ratio of the intimal area to the medial area (36.2%) in injured arteries compared with those of control rats at 14 days after the injury. Real-time RT-PCR, Western blot, and gelatin zymography revealed a significant increase in tissue inhibitor of matrix metalloproteinase (MMP)-2 (TIMP-2) expression as well as a significant reduction of gelatinolytic net activity and activated MMP-2 levels in the injured arteries as a result of the administration of the tea extract compared with those of control group. Similarly, epigallocatechin-3-gallate, a major constituent of green tea catechins, significantly upregulated TIMP-2 expression in cultured smooth muscle cells. Immunohistochemical analysis showed that the increase of TIMP-2 protein occurred preferentially in the developing neointima. CONCLUSION: These results indicate that catechins inhibit intimal hyperplasia in a rat balloon-injury model through the upregulation of TIMP-2 expression to modulate MMP activity.     

An in vitro hyperbaric oxygen system for evaluation of free radical damage and protection by catechins on hemorheological parameters

Free radicals play a critical role in causing hemorheologic abnormality which is highly correlated with cardiovascular disease and stroke. In this study, we established an in vitro model to evaluate the influence of free radical attacks on hemorheological parameters. A well-sealed chamber with hyperbaric oxygen was used to simulate an environment of free radical attacks. Hemorheological parameters, including whole blood viscosity, erythrocyte membrane lipid peroxidation, and erythrocyte deformability, were investigated. We then used the in vitro model to evaluate the anti-free radical effects of some well-known catechin antioxidants, such as epigallocatechin gallate (EGCG), (-)-epicatechin 3-gallate (ECG), and (-)-epigallocatechin (EGC) on abnormal hemorheological parameters induced by hyperbaric oxygen. The results show that an increase in oxygen partial pressure (1.0, 1.5, 2.0 and 2.5 atm) and exposure time (4, 8, 12 and 16 h) resulted in elevated free radical formation and viscosity of whole blood, enhanced lipid peroxidation in erythrocyte membranes, but decreased erythrocyte deformability. In addition, EGCG, ECG, and EGC (0.1, 0.5 and 1.0 μM) effectively ameliorated hemorheologic abnormality and enhanced erythrocyte deformability. Therefore, this study has provided an in vitro hyperbaric oxygen model to rapidly screen or assess the efficacy of functional foods and drugs in the prevention or improvement of hemorheologic abnormality.     

Therapeutic potential of green tea on risk factors for type 2 diabetes in obese adults – a review

Green tea has been associated with positive effects in the treatment of obesity and other associated comorbidities such as type 2 diabetes. These benefits are thought to be related to the anti‐inflammatory and antioxidant effects of green tea and to the reduction in body fat percentage exhibited by its bioactive compounds. The predominant active compounds in green tea are flavonoid monomers known as catechins, in particular epigallocatechin‐3‐gallate, which is the most abundant and most effective catechin in metabolic care, particularly among obese patients. The objective of this review was to investigate the effects of green tea on body composition, oxidative stress, inflammation and insulin resistance, risk factors for the development of type 2 diabetes in obese individuals and the mechanisms that underlie the modulatory actions of green tea compounds on these risk factors. Although green tea has therapeutic potential in the treatment of obese individuals, the findings of this review demonstrate the need for a greater number of studies to confirm the positive effects of green tea, especially regarding the modulation of obesity.