Effect Of Epigallocatechin-3-O-gallate Research Articles

(−)-Epigallocatechin-3-O-gallate or (−)-epicatechin enhances lipid catabolism and antioxidant defense in common carp (Cyprinus carpio L.) fed a high-fat diet: Mechanistic insights from the AMPK/Sirt1/PGC-1α signaling pathway

Long-term high-fat diets (HF) lead to lipid accumulation and an oxidative stress response, which deteriorates the chemical and physical characteristics of fish muscle. Green tea extracts, such as (−)-epigallocatechin-3-O-gallate (EGCG) and (−)-epicatechin (EC), have been found to regulate antioxidant ability and lipid metabolism. However, the effects of EGCG and EC on alleviating oxidative stress and lipid metabolism disorders caused by HF are unclear. Furthermore, the underlying mechanisms remain unknown. In this study, a total of 360 carp (average weight: 9.75 ± 0.09 g) were provided with four experimental diets: a control diet (CN, 6.15% dietary lipids), a high-fat diet (HF, 14.05% dietary lipids), HF supplemented with EGCG (HF + EGCG, 14.05% dietary lipids +50 mg/kg EGCG), and a HF diet supplemented with EC (HF + EC, 14.05% dietary lipids +1000 mg/kg EC) for a duration of 84 days. The results indicated that EGCG or EC ameliorated the negative effects of the HF diet on muscle tissue. Apart from muscle physical characteristics, EGCG decreased yellowness (b*), redness (a*), and dripping loss (P < 0.05). Apart from muscle nutritional composition and antioxidant status, EC mitigated the reduction in protein levels in the muscle induced by the HF diet. Similarly, EGCG and EC mitigated the excessive accumulation of lipids and reactive oxygen species (ROS) in the muscle induced by the HF diet (P < 0.05). Further study showed that EGCG or EC facilitated the phosphorylation of AMP-activated protein kinase (AMPK) and increased silent information regulator 1 (Sirt1) and PPARγ coactivator-1 alpha (PGC-1α) expression in muscle. Taken together, the results of this study revealed that EGCG or EC enhance lipid metabolism and antioxidant capacity in the muscle of common carp (Cyprinus carpio L.) via the AMPK/Sirt1/PGC-1α pathway.

The anti-cancer effect of epigallocatechin-3-O-gallate against multiple myeloma cells is potentiated by 5,7-dimethoxyflavone.

(-)-Epigallocatechin-3-O-gallate (EGCG) is one of the major components of green tea polyphenol. Previous studies have shown that EGCG induces cancer-specific cell death in vitro and in vivo without causing severe side effects. However, the anti-cancer effect of EGCG alone is limited. 5,7-dimethoxyflavone (5,7-DMF), one of the principal functional components of black ginger (Kaempferia parviflora), also exerts anti-cancer effects. Here, we show that 5,7-DMF synergistically enhances the anti-cancer effect of EGCG in multiple myeloma cells by potentiating EGCG-induced intracellular cyclic guanosine monophosphate (cGMP) production. Moreover, the combination of EGCG and 5,7-DMF induces apoptotic cell death in multiple myeloma cells, and this is accompanied by activation of the cGMP/acid sphingomyelinase (ASM)/cleaved caspase-3 pathway. In conclusion, we have shown that 5,7-DMF enhances the anti-cancer effect of EGCG by upregulating cGMP in multiple myeloma cells.

(-)-Epigallocatechin-3-Gallate Prevents IL-1β-Induced uPAR Expression and Invasiveness via the Suppression of NF-κB and AP-1 in Human Bladder Cancer Cells.

(-)-Epigallocatechin-3-O-gallate (EGCG), a primary green tea polyphenol, has powerful iron scavengers, belongs to the family of flavonoids with antioxidant properties, and can be used to prevent cancer. Urokinase-type plasminogen activator receptors (uPARs) are glycosylphosphatidylinositol (GPI)-anchored cell membrane receptors that have crucial roles in cell invasion and metastasis of several cancers including bladder cancer. The mechanism of action of EGCG on uPAR expression has not been reported clearly yet. In this study, we investigated the effect of EGCG on interleukin (IL)-1β-induced cell invasion and uPAR activity in T24 human bladder cancer cells. Interestingly, nuclear factor (NF)-κB and activator protein (AP)-1 transcription factors were critically required for IL-1β-induced high uPAR expression, and EGCG suppressed the transcriptional activity of both the ERK1/2 and JNK signaling pathways with the AP-1 subunit c-Jun. EGCG blocked the IL-1β-stimulated reactive oxygen species (ROS) production, in turn suppressing NF-κB signaling and anti-invasion effects by inhibiting uPAR expression. These results suggest that EGCG may exert at least part of its anticancer effect by controlling uPAR expression through the suppression of ERK1/2, JNK, AP-1, and NF-κB.

67-kDa Laminin Receptor-Mediated Cellular Sensing System of Green Tea Polyphenol EGCG and Functional Food Pairing.

The body is equipped with a “food factor-sensing system” that senses food factors, such as polyphenols, sulfur-containing compounds, and vitamins, taken into the body, and plays an essential role in manifesting their physiological effects. For example, (−)-epigallocatechin-3-O-gallate (EGCG), the representative catechin in green tea (Camellia sinensi L.), exerts various effects, including anti-cancer, anti-inflammatory, and anti-allergic effects, when sensed by the cell surficial protein 67-kDa laminin receptor (67LR). Here, we focus on three representative effects of EGCG and provide their specific signaling mechanisms, the 67LR-mediated EGCG-sensing systems. Various components present in foods, such as eriodictyol, hesperetin, sulfide, vitamin A, and fatty acids, have been found to act on the food factor-sensing system and affect the functionality of other foods/food factors, such as green tea extract, EGCG, or its O-methylated derivative at different experimental levels, i.e., in vitro, animal models, and/or clinical trials. These phenomena are observed by increasing or decreasing the activity or expression of EGCG-sensing-related molecules. Such functional interaction between food factors is called “functional food pairing”. In this review, we introduce examples of functional food pairings using EGCG.

Multi-target Approaches of Epigallocatechin-3-O-gallate (EGCG) and its Derivatives against Influenza Viruses.

Influenza viruses (INFV), the Orthomyxoviridae family, are mainly transmitted among humans via aerosols or droplets from the respiratory secretions. However, fomites could be a potential transmission pathway. Annually, seasonal INFV infections account for 290-650 thousand deaths worldwide. Currently, there are two classes of approved drugs to treat INFV infections, being neuraminidase (NA) inhibitors and blockers of matrix-2 (M2) ion channel. However, cases of resistance have been observed for both chemical classes, reducing the efficacy of treatment. The emergence of influenza outbreaks and pandemics calls for new antiviral molecules that are more effective, and that could overcome the current resistance to anti-influenza drugs. In this context, polyphenolic compounds are found in various plants, and these have displayed different multi-target approaches against diverse pathogens. Among these, green tea (Camellia sinensis) catechins, in special epigallocatechin-3-O-gallate (EGCG), have demonstrated significant activities against the two most relevant human INFV, subtypes A and lineages B. In this sense, EGCG has been found to be a promising multi-target agent against INFV since it can act inhibiting NA, hemagglutination (HA), RNA-dependent RNA polymerase (RdRp), and viral entry/adsorption. In general, the lack of knowledge about potential multi-target natural products prevents an adequate exploration of them, increasing the time for developing multi-target drugs. Then, this review aimed to compile most relevant studies showing the anti-INFV effects of EGCG and its derivatives, which could become antiviral drug prototypes in the future.

Epigallocatechin-3-O-gallate ameliorates oxidative stress-induced chondrocyte dysfunction and exerts chondroprotective effects via the Keap1/Nrf2/ARE signaling pathway.

Oxidative stress-induced degeneration and dysfunction of chondrocytes play a key role in the pathological progression of osteoarthritis (OA), a common degenerative joint disease in the elderly. Epigallocatechin-3-O-gallate (EGCG) increases Nrf2-mediated antioxidase expression levels. We aimed to determine the effects of EGCG on C28/I2human chondrocytes subjected to interleukin-1β (IL-1β)-induced oxidative stress. EGCG suppressed IL-1β-induced oxidative stress, as indicated by decreased malondialdehyde (MDA) and reactive oxygen species (ROS) generation. Additionally, EGCG attenuated the IL-1β-induced reduction in cartilage matrix generated by chondrocytes by upregulating collagen II, aggrecan, sulfated proteoglycans, and SRY-box transcription factor 9 (SOX9). EGCG reversed the IL-1β-induced increased cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), collagen X, and matrix metalloproteinases (MMPs). Furthermore, EGCG inhibited apoptosis and senescence of IL-1β-treated chondrocytes, as indicated by the decrease in mitochondrial membrane potential and senescence-associated β-galactosidase-positive cells, respectively. Mechanically, EGCG upregulated nuclear factor erythroid 2-related factor 2 (Nrf2), oxygenase-1 (HO-1), and NADPH quinone oxidoreductase1 (NQO1). The antioxidant and chondroprotective effects of EGCG were blocked by ML385, a Keap1/Nrf2/ARE signaling pathway inhibitor. Thus, EGCG ameliorated oxidative stress-induced chondrocyte dysfunction and exerted chondroprotective effects via Keap1/Nrf2/ARE signaling. This provides a novel perspective on the molecular mechanisms underlying the therapeutic effects of EGCG on OA.

Fustin, a Flavanonol, Synergically Potentiates the Anticancer Effect of Green Tea Catechin Epigallocatechin-3-O-Gallate with Activation of the eNOS/cGMP Axis.

Epigallocatechin-3-O-gallate (EGCG), a catechin present in green tea, selectively elicits apoptosis in multiple myeloma cells by activating the endothelial nitric oxide synthase (eNOS)/cyclic guanosine monophosphate (cGMP) axis. However, the effects of EGCG alone are limited. Herein, we revealed that fustin, a flavanonol, enhances the EGCG-elicited activation of the cGMP/eNOS axis in multiple myeloma cells. Isobologram analysis demonstrated that EGCG/fustin synergistically elicited cell death in multiple myeloma cells. Importantly, this chemical combination significantly promoted cell death without affecting the normal cells. To assess the effects of EGCG and fustin in vivo, female BALB/c mice were inoculated with multiple myeloma MPC11 cells and then treated with each compound. The combination of EGCG/fustin suppressed tumor growth in vivo without affecting alanine aminotransferase/aspartate aminotransferase levels, the dose-limiting toxicity of EGCG. Consistent with in vitro findings, this combination increased eNOS phosphorylation at Ser1177 in the tumor. Collectively, fustin amplified EGCG-induced activation of the eNOS/cGMP axis.

Antiviral Effects of Green Tea EGCG and Its Potential Application against COVID-19.

(–)-Epigallocatechin-3-O-gallate (EGCG), the most abundant component of catechins in tea (Camellia sinensis (L.) O. Kuntze), plays a role against viruses through inhibiting virus invasiveness, restraining gene expression and replication. In this paper, the antiviral effects of EGCG on various viruses, including DNA virus, RNA virus, coronavirus, enterovirus and arbovirus, were reviewed. Meanwhile, the antiviral effects of the EGCG epi-isomer counterpart (+)-gallocatechin-3-O-gallate (GCG) were also discussed.

Glucosyl-hesperidin enhances the cyclic guanosine monophosphate-inducing effect of a green tea polyphenol EGCG.

Animal and clinical studies have revealed that (-)-epigallocatechin-3-O-gallate (EGCG), one of the major bioactive polyphenols in green tea, showed several pharmacological effects including anti-obesity effect and anti-inflammatory effect. We previously reported that the second messenger cyclic guanosine monophosphate (cGMP) mediates its anti-inflammatory and anti-cancer properties. Here we demonstrated that glucosyl-hesperidin, enhances the cGMP-inducing effects of green tea extract in vivo. Moreover, glucosyl-hesperidin intake potentiated the green tea-elicited upregulation of the anti-inflammatory factor, toll-interacting protein.

Epigallocathechin-O-3-Gallate Inhibits Trypanothione Reductase of Leishmania infantum, Causing Alterations in Redox Balance and Leading to Parasite Death.

Leishmania infantum is a protozoan parasite that causes a vector borne infectious disease in humans known as visceral leishmaniasis (VL). This pathology, also caused by L. donovani, presently impacts the health of 500,000 people worldwide, and is treated with outdated anti-parasitic drugs that suffer from poor treatment regimens, severe side effects, high cost and/or emergence of resistant parasites. In previous works we have disclosed the anti-Leishmania activity of (-)-Epigallocatechin 3-O-gallate (EGCG), a flavonoid compound present in green tea leaves. To date, the mechanism of action of EGCG against Leishmania remains unknown. This work aims to shed new light into the leishmanicidal mode of action of EGCG. Towards this goal, we first confirmed that EGCG inhibits L. infantum promastigote proliferation in a concentration-dependent manner. Second, we established that the leishmanicidal effect of EGCG was associated with i) mitochondria depolarization and ii) decreased concentration of intracellular ATP, and iii) increased concentration of intracellular H2O2. Third, we found that the leishmanicidal effect and the elevated H2O2 levels induced by of EGCG can be abolished by PEG-catalase, strongly suggesting that this flavonoid kills L. infantum promastigotes by disturbing their intracellular redox balance. Finally, we gathered in silico and in vitro evidence that EGCG binds to trypanothione reductase (TR), a central enzyme of the redox homeostasis of Leishmania, acting as a competitive inhibitor of its trypanothione substrate.

Time-dependent increase of plasma cGMP concentration followed by oral EGCG administration in mice

Epigallocatechin 3-O-gallate (EGCG), the major catechin in green tea, exerts several beneficial effects in vivo. A previous study showed that cyclic guanosine monophosphate (cGMP) as a cellular second messenger has been shown to be an important mediator of the effects of EGCG. In general, long-term animal experiments are required to evaluate the functionality of phytochemicals such as EGCG. Thus, it might be beneficial to establish a marker for short-term evaluation of functional phytochemicals. In this study, the use of the plasma cGMP level was evaluated as a surrogate marker for the functional effectiveness of EGCG. Blood samples were collected from 6-wk-old C57BL/6J mice from 1 to 8 h after oral administration of EGCG (30 or 100 mg/kg). The upregulation of plasma cGMP levels elicited by the oral EGCG administration was evaluated. Additionally, it was confirmed that EGCG induced the expressions of intracellular Toll interacting protein (Tollip), which is mainly controlled by a cGMP signal in the spleen. These data indicated that the plasma cGMP levels could be a screening marker for the effect of EGCG.

Interindividual Differences in Human In Vitro Intestinal Microbial Conversion of Green Tea (‐)‐Epigallocatechin‐3‐O‐Gallate and Consequences for Activation of Nrf2 Mediated Gene Expression

ScopeAn in vitro faecal incubation model combined with reporter gene assay based testing strategy is developed to characterize interindividual differences in the gut microbial conversion of (‐)‐epigallocatechin‐3‐O‐gallate (EGCG) and its consequences for potential activation of Nrf2‐mediated gene expression.Method & ResultsAnaerobic human faecal incubations are performed to characterize the microbial metabolism of EGCG including interindividual variability. EGCG derived intestinal microbial metabolite patterns show substantial interindividual differences that are correlated to relative microbial abundances determined by 16S rRNA sequencing. Results obtained show the time‐dependent formation of gallic acid, pyrogallol, phenylpropane‐2‐ols, phenyl‐γ‐valerolactones, and 5‐(3′,5′‐dihydroxyphenyl)valeric acid as the major metabolites, with substantial interindividual differences. The activity of the formed metabolites in the activation of EpRE‐mediated gene expression is tested by EpRE‐LUX reporter gene assay. In contrast to EGCG, at low micromolar concentrations, especially gallic acid, pyrogallol, and catechol induce significant activity in the EpRE‐LUX assay.ConclusionsGiven these results and taking the level of formation into account, it is concluded that especially gallic acid and pyrogallol contribute to the EpRE‐mediated beneficial effects of EGCG. The interindividual differences in the formation may result in interindividual differences in the beneficial effects of EGCG and green tea consumption.

Src Mediates Epigallocatechin-3-O-Gallate-Elicited Acid Sphingomyelinase Activation.

Epigallocatechin-3-O-gallate (EGCG) is one of the major bioactive compounds known to be present in green tea. We previously reported that EGCG shows selective toxicity through activation of the protein kinase B (Akt)/cyclic guanosine monophosphate (cGMP)/acid sphingomyelinase (ASM) axis via targeting its receptor 67-kDa laminin receptor (67LR), which is overexpressed in cancer. However, little is known about upstream mechanisms of EGCG-elicited ASM activation. In this study we show that the proto-oncogene tyrosine-protein kinase Src, also known as c-src, plays a crucial role in the anticancer effect of EGCG. We showed that EGCG elicits phosphorylation of Src at Tyr 416, a crucial phosphorylation site for its activity, and that the pharmacological inhibition of Src impedes the upstream events in EGCG-induced cell death signaling including upregulation of Akt activity, increase in cGMP levels, and activation of ASM. Moreover, focal adhesion kinase (FAK), which is involved in the phosphorylation of Src, is colocalized with 67LR. EGCG treatment enhanced interaction of FAK and 67LR. Consistent with these findings, pharmacological inhibition of FAK significantly neutralized EGCG-induced upregulation of Akt activity and activation of ASM. Taken together, FAK/Src play crucial roles in the upstream signaling of EGCG.

Epigallocatechin-3-Gallate and PEDF 335 Peptide, 67LR Activators, Attenuate Vasogenic Edema, and Astroglial Degeneration Following Status Epilepticus.

Non-integrin 67-kDa laminin receptor (67LR) is involved in cell adherence to the basement membrane, and it regulates the interactions between laminin and other receptors. The dysfunction of 67LR leads to serum extravasation via blood-brain barrier (BBB) disruption. Polyphenol (–)-epigallocatechin-3-O-gallate (EGCG) and pigment epithelium-derived factor (PEDF) bind to 67LR and inhibit neovascularization. Therefore, in the present study, we investigated the effects of EGCG and NU335, a PEDF-derive peptide, on BBB integrity and their possible underlying mechanisms against vasogenic edema formation induced by status epilepticus (SE, a prolonged seizure activity). Following SE, both EGCG and NU335 attenuated serum extravasation and astroglial degeneration in the rat piriform cortex (PC). Both EGCG and NU335 reversely regulated phosphatidylinositol 3 kinase (PI3K)/AKT–eNOS (endothelial nitric oxide synthase) mediated BBB permeability and aquaporin 4 (AQP4) expression in endothelial cells and astrocytes through the p38 mitogen-activated protein kinase (p38 MAPK) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathways, respectively. Furthermore, EGCG and NU335 decreased p47Phox (a nicotinamide adenine dinucleotide phosphate oxidase subunit) expression in astrocytes under physiological and post-SE conditions. Therefore, we suggest that EGCG and PEDF derivatives may activate 67LR and its downstream effectors, and they may be considerable anti-vasogenic edema agents.

67-kDa Laminin Receptor Mediates the Beneficial Effects of Green Tea Polyphenol EGCG

Green tea is one of the most consumed beverages in the world. Through in vivo models and clinical trials, several studies have shown the beneficial effects of green tea. Epidemiological studies have revealed that green tea consumption is negatively correlated with the risk of cardiovascular diseases, stroke and cancer; however, little is known about the underlying molecular mechanisms. (−)-Epigallocatechin-3-O-gallate (EGCG) is one of the major bioactive compounds in green tea, and several studies emphasise its central role in the beneficial effects of green tea. It has been demonstrated that the 67-kDa laminin receptor, a non-integrin laminin receptor, mediates the beneficial effects of EGCG through cyclic guanosine monophosphate–dependent mechanisms. In this review, we showed the role of 67LR as the sensor of the EGCG and its downstream cascade, and this review provides the recent findings in the mechanism of the beneficial effect of EGCG.

Antidepressant effect of EGCG through the inhibition of hippocampal neuroinflammation in chronic unpredictable mild stress-induced depression rat model

Abstract In our study, a chronic unpredictable mild stress-induced depression rat model was constructed then the antidepressant effects and mechanisms of Epigallocatechin-3-O-gallate (EGCG) have been evaluaed accordingly. In the study, there were three subgroups of stochastically-selected male Wistar rats, namely, Control, CUMS-induced (chronic unpredictable mild stress) and CUMS with EGCG administration. The outcomes of sucrose preference and open-field tests presented the antidepressant-like effects of EGCG. With EGCG treatment, the levels of IL-6 and NO had significantly declined. Through EGCG administration, the suppressed expression of caspase-3 and caspase-9 mRNA in hippocampus was exhibited in the experiment. The implication of experimental outcomes can be served as preclinical evidences for therapeutic applications in the treatment of depression potentially, because of the antidepressant-like role of EGCG played against inflammation to protect neurons in hippocampus.

EGCG down-regulates MuRF1 expression through 67-kDa laminin receptor and the receptor signaling is amplified by eriodictyol.

(-)-epigallocatechin-3-O-gallate (EGCG) is a bioactive polyphenol in green tea. Previous studies have demonstrated the beneficial effects of EGCG on muscle mass and muscle atrophy. In the current study, we investigated the mechanisms underlying effect of EGCG on muscle atrophy. It was demonstrated that EGCG suppressed muscle-specific ubiquitin ligase, muscle RING Finger 1 (MuRF1) expression through 67-kDa laminin receptor (67LR). Previous studies have shown that eriodictyol potentiates the anti-tumor activities of EGCG by amplifying 67LR signaling. Therefore, we investigated the effects of EGCG and eriodictyol on the MuRF1 expression in C2C12 myotubes. The combined treatment of EGCG and eriodictyol significantly suppressed MuRF1 expression in dexamethasone-treated C2C12 myotubes. Tail suspension was maintained for 10 consecutive days using C57BL6/J mice, and during this time EGCG and eriodictyol were orally administered. In the gastrocnemius muscle, the muscle mass loss was inhibited by the combination of EGCG and eriodictyol. Therefore, EGCG may prevent muscle atrophy by inducing 67LR signaling and eriodictyol amplifies this pathway.

Epigallocatechin-3-O-gallate induces acid sphingomyelinase activation through activation of phospholipase C

Epigallocatechin-3-O-gallate (EGCG)-induced cyclic guanosine monophosphate (cGMP) plays a crucial role in EGCG-induced cell death in various types of cancer cells. However, little is known regarding the early molecular events after cGMP induction. In this study, we showed that cGMP induction is sufficient to induce the phosphorylation of protein kinase C delta (PKCδ) at Ser664, the crucial kinase for EGCG-induced activation of acid sphingomyelinase (ASM). Using a chemical inhibitor library, we revealed that the inhibitors of the negative regulators of diacylglycerol strongly increase the effect of EGCG. We also showed that EGCG treatment increased phospholipase C (PLC) activity, and the same results were obtained with cGMP inducer treatment. EGCG-induced ASM activation was completely suppressed by pharmacological inhibition of PLC. Collectively, EGCG-induced cGMP activated the cGMP/PLC/PKCδ/ASM signaling axis in multiple myeloma cells.

Inhibitory effect of epigallocatechin-3-O-gallate on α-glucosidase and its hypoglycemic effect via targeting PI3K/AKT signaling pathway in L6 skeletal muscle cells

Epigallocatechin-3-O-gallate (EGCG), a tea polyphenol is renowned for its anti-diabetic properties, however limited studies elucidate its hypoglycemic mechanism from multi-perspectives. In the present study, the interaction between EGCG and α-glucosidase was investigated through kinetics analysis, fluorescence spectra, Fourier transform infrared (FT-IR) spectra and molecular docking studies. Additionally, the effect of EGCG on glucose uptake and its related signaling pathway in L6 muscle cells were also investigated. The results showed that the α-glucosidase inhibitory activity of EGCG (IC50 = 19.5 ± 0.3 μM) was higher than that acarbose (IC50 = 278.7 ± 1.1 μM). EGCG inhibited α-glucosidase in a reversible and non-competitive manner. EGCG quenched the fluorescence of α-glucosidase due to the complex formation between EGCG and α-glucosidase, where the hydrogen bonds played a critical role. Microenvironment and the secondary structure of α-glucosidase were highly influenced by EGCG. Molecular docking results indicated that the binding sites on α-glucosidase for EGCG were close to the active site pocket of the enzyme. EGCG was also found to enhance the glucose uptake and promote GLUT4 translocation to plasma membrane via PI3K/AKT signaling pathway in L6 skeletal muscle cells. Overall, these results revealed the possible hypoglycemic mechanism of EGCG.

Saturated fatty acid attenuates anti-obesity effect of green tea

Green tea and its major polyphenol epigallocatechin-3-O-gallate (EGCG) have suppressive effect on dietary obesity. However, it remains unsolved what type of diet on which they exhibit high or low anti-obesity effect. In the present study, we investigated whether anti-obesity effect of green tea differs depending on composition of fats or fatty acids that consist high-fat (HF) diet in mouse model. Green tea extract (GTE) intake dramatically suppressed weight gain and fat accumulation induced by olive oil-based HF diet, whereas the effects on those induced by beef tallow-based HF diet were weak. GTE also effectively suppressed obesity induced by unsaturated fatty acid-enriched HF diet with the stronger effect compared with that induced by saturated fatty acid-enriched HF diet. These differences would be associated with the increasing action of GTE on expression of PPARδ signaling pathway-related genes in the white adipose tissue. Expressions of genes relating to EGCG signaling pathway that is critical for exhibition of physiological effects of EGCG were also associated with the different effects of GTE. Here, we show that anti-obesity effect of GTE differs depending on types of fats or fatty acids that consist HF diet and could be attenuated by saturated fatty acid.