Catechin-rich Green Tea Extract Research Articles

A green tea extract confection decreases circulating endotoxin and fasting glucose by improving gut barrier function but without affecting systemic inflammation: A double-blind, placebo-controlled randomized trial in healthy adults and adults with metabolic syndrome

Anti-inflammatory activities of catechin-rich green tea extract (GTE) in obese rodents protect against metabolic endotoxemia by decreasing intestinal permeability and absorption of gut-derived endotoxin. However, translation to human health has not been established. We hypothesized that GTE would reduce endotoxemia by decreasing gut permeability and intestinal and systemic inflammation in persons with metabolic syndrome (MetS) compared with healthy persons. A randomized, double-blind, placebo-controlled, crossover trial in healthy adults (n = 19, 34 ± 2 years) and adults with MetS (n = 21, 40 ± 3 years) examined 4-week administration of a decaffeinated GTE confection (890 mg/d total catechins) on serum endotoxin, intestinal permeability, gut and systemic inflammation, and cardiometabolic parameters. Compared with the placebo, the GTE confection decreased serum endotoxin (P = .023) in both healthy persons and those with MetS, while increasing concentrations of circulating catechins (P < .0001) and γ-valerolactones (P = .0001). Fecal calprotectin (P = .029) and myeloperoxidase (P = .048) concentrations were decreased by GTE regardless of health status. Following the ingestion of gut permeability probes, urinary lactose/mannitol (P = .043) but not sucralose/erythritol (P > .05) was decreased by GTE regardless of health status. No between-treatment differences (P > .05) were observed for plasma aminotransferases, blood pressure, plasma lipids, or body mass nor were plasma tumor necrosis factor-α, interleukin-6, or the ratio of lipopolysaccharide-binding protein/soluble cluster of differentiation-14 affected. However, fasting glucose in both study groups was decreased (P = .029) by the GTE confection compared with within-treatment arm baseline concentrations. These findings demonstrate that catechin-rich GTE is effective to decrease circulating endotoxin and improve glycemic control in healthy adults and those with MetS, likely by reducing gut inflammation and small intestinal permeability but without affecting systemic inflammation.

Induction of mitophagy by green tea extracts and tea polyphenols: A potential anti-aging mechanism of tea

Tea consumption has been associated with anti-aging effects, however, the mechanisms involved are not well understood. Prompting mitochondrial health via the induction of mitophagy has recently been proposed as a novel anti-aging mechanism and the anti-aging properties of a few polyphenols including urolithin A have been linked to their abilities to induce mitophagy. Teas, rich in polyphenols, may also produce anti-aging effects through the induction of mitophagy. To test this hypothesis, a green tea extract and a few common tea polyphenols (catechins), were evaluated as potential mitophagy inducers in normal human fibroblasts. Mitophagy was detected by confocal microscopy and confirmed by Western blot analysis. A catechin-rich green tea extract (polyphenol content of 98%) induced mitophagy in normal human fibroblasts in a dose-dependent manner with a maximum effective concentration at ∼5 μg/mL, demonstrating comparable efficacy to urolithin A. Tea catechins also induced similar levels of mitophagy at an effective concentration of 5 μM for (-)-epicatechin gallate, EGCG and (-)-epicatechin, and 10 μM for (+)-catechin and (-)-epigallocatechin. These results demonstrate that the polyphenols in teas are powerful inducers of mitophagy in human fibroblast cells and induction of mitophagy may play an important role in the anti-aging mechanism of teas.

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

Abstract Objectives Preclinical evidence demonstrated that catechin-rich green tea extract (GTE) improves gut barrier function and reduces intestinal and systemic inflammation. Thus, this clinical trial was conducted to test the hypothesis that GTE would alleviate intestinal inflammation relative to cardiometabolic risk in persons with metabolic syndrome (MetS). Methods We conducted a randomized, double-blind, placebo-controlled, crossover trial in adults with MetS and age- and gender-matched healthy persons who received confections without (placebo) or with 1 g/d GTE (890 mg catechins) for 28 d while following a low-polyphenol diet. Dietary polyphenols, fasting blood glucose, insulin, and lipids were assessed at d 0, 14, and 28 of each intervention. Intestinal inflammation was assessed by measuring neutrophil-derived calprotectin and myeloperoxidase by ELISA in pooled stool samples collected over the last 3 d of each intervention. Data were analyzed using RM ANOVA and multiple linear regression. Results MetS (n = 21; 40 ± 3 y; 35 ± 1 kg/m2) and healthy (n = 19; 34 ± 2 y; 22 ± 0.4 kg/m2) persons completed the study with high compliance (&amp;gt;95%), no adverse effects, or changes in body mass. Participants’ total polyphenol intakes decreased during each intervention compared with baseline (P &amp;lt; 0.001). Fecal calprotectin and myeloperoxidase were lower (P &amp;lt; 0.05) in GTE compared with placebo regardless of health status. Although fasting insulin, triglycerides, total and high-density lipoprotein cholesterol were unaffected by treatment, fasting glucose decreased (P &amp;lt; 0.01) in response to GTE regardless of health status. Age (β = −0.29; P = 0.05) and between-trial changes in myeloperoxidase (β = 0.03; P &amp;lt; 0.04) were predictive of changes in insulin after controlling for sex, waist circumference, and changes in blood lipids and calprotectin. Conclusions Dietary intervention with GTE-rich confections in weight-stable healthy and MetS adults decreased fasting glucose and intestinal inflammation, which was associated with improvements in fasting insulin. This suggests that gut-level anti-inflammatory activities of GTE may improve glycemic control with reductions in intestinal inflammation contributing to enhance insulin sensitivity. Funding Sources USDA-NIFA, USDA-HATCH, and the Ohio Agricultural Research and Development Center at the Ohio State University.

A Green Tea Extract-Rich Confection in Healthy and Metabolic Syndrome Adults Decreases Small Intestinal Permeability in Association With Lower Gut Inflammation

ObjectivesPoor gut health, including increased intestinal permeability and inflammation, enhances cardiometabolic risk. Catechin-rich green tea extract (GTE) alleviates cardiometabolic complications in obese rodents by limiting gut permeability and inflammation, but whether these benefits occur in humans is not known. We hypothesized that the anti-inflammatory activities of GTE would decrease gut barrier dysfunction in persons at heightened cardiometabolic risk. MethodsIn a randomized, double-blind, placebo-controlled crossover study, persons with metabolic syndrome (MetS) and healthy persons completed two 4-wk interventions in which they received placebo or GTE confections (890 mg/d total catechins) while following a low-polyphenol diet. At wk 4, participants provided fecal samples for ELISA-based measures of inflammatory proteins. 24-h urine samples were also collected for LC/MS analysis of non-digestible sugars following the ingestion of lactulose (LAC), mannitol (MAN), sucralose (SUC), and erythritol (ERY). Data were analyzed by repeated measures ANOVA and linear regression controlling for within-subject repeated measures. ResultsMetS (n = 21; 40 ± 3 y; 35.2 ± 1.0 kg/m2) and healthy (n = 19; 34 ± 2 y; BMI = 22.3 ± 0.4 kg/m2) adults completed the study with no adverse effects, no changes in liver function tests, and > 95% compliance based on returned confections. Urinary SUC/ERY was unaffected by GTE and health status, but urinary LAC/MAN was lower (P = 0.043) in GTE compared with placebo regardless of health status. Fecal myeloperoxidase and calprotectin did not differ by health status, but were lower (P = 0.03–0.05) in response to GTE regardless of health status, and were positively correlated with each other (r = 0.75; P < 0.001). Fecal calprotectin and myeloperoxidase were both positively correlated with LAC/MAN ratio (r = 0.39–0.42; P = 0.01–0.02). ConclusionsInterim findings of this study support that dietary GTE decreases small intestinal permeability in association with lower gut inflammation, which may help to explain its known cardiometabolic benefits. Funding SourcesUSDA-NIFA (2019–67,017-29,259), USDA-HATCH, and the Ohio Agricultural Research and Development Center at The Ohio State University.

Prophylactic Catechin-Rich Green Tea Extract Treatment Ameliorates Pathogenic Enterotoxic Escherichia coli-Induced Colitis.

In this study, we explored the potential beneficial effects of green tea extract (GTE) in a pathogenic Escherichia coli (F18:LT:STa:Stx2e)-induced colitis model. The GTE was standardized with catechin and epigallocatechin-3-gallate content using chromatography analysis. Ten consecutive days of GTE (500 and 1000 mg/kg) oral administration was followed by 3 days of a pathogenic E. coli challenge (1 × 109 CFU/mL). In vitro antibacterial analysis showed that GTE successfully inhibited the growth of pathogenic E. coli, demonstrating over a 3-fold reduction under time- and concentration-dependent conditions. The in vivo antibacterial effect of GTE was confirmed, with an inhibition rate of approximately 90% when compared to that of the E. coli alone group. GTE treatment improved pathogenic E. coli-induced intestinal injury with well-preserved epithelial linings and villi. In addition, the increased expression of annexin A1 in GTE-treated jejunum tissue was detected, which was accompanied by suppressed inflammation-related signal expression, including TNFA, COX-2, and iNOS. Moreover, proliferation-related signals such as PCNA, CD44, and Ki-67 were enhanced in the GTE group compared to those in the E. coli alone group. Taken together, these results indicate that GTE has an antibacterial activity against pathogenic E. coli and ameliorates pathogenic E. coli-induced intestinal damage by modulating inflammation and epithelial cell proliferation.

Catechin-Rich Green Tea Extract and the Loss-of-TLR4 Signaling Differentially Alter the Hepatic Metabolome in Mice with Nonalcoholic Steatohepatitis.

Catechin-rich green tea extract (GTE) limits inflammation in nonalcoholic steatohepatitis (NASH) consistent with a Toll-like receptor 4 (TLR4)-dependent mechanism. It is hypothesized that GTE supplementation during NASH will shift the hepatic metabolome similar to that attributed to the loss-of-TLR4 signaling. Wild-type (WT) and loss-of-function TLR4-mutant (TLR4mut ) mice are fed a high-fat diet containing 0% or 2% GTE for 8 weeks prior to performing untargeted mass spectrometry-based metabolomics on liver tissue. The loss-of-TLR4 signaling and GTE shift the hepatic metabolome away from that of WT mice. However, relatively few metabolites are altered by GTE in WT mice to the same extent as the loss-of-TLR4 signaling in TLR4mut mice. GTE increases acetyl-coenzyme A precursors and spermidine to a greater extent than the loss-of-TLR4 signaling. Select metabolites associated with thiol metabolism are similarly affected by GTE and the loss-of-TLR4 signaling. Glycerophospholipid catabolites are decreased by GTE, but are unaffected in TLR4mut mice. Conversely, the loss-of-TLR4 signaling but not GTE increases several bile acid metabolites. GTE limitedly alters the hepatic metabolome consistent with a TLR4-dependent mechanism. This suggests that the anti-inflammatory activities of GTE and loss-of-TLR4 signaling that regulate hepatic metabolism to abrogate NASH are likely due to distinct mechanisms.

Epigallocatechin gallate but not catechin prevents nonalcoholic steatohepatitis in mice similar to green tea extract while differentially affecting the gut microbiota

Catechin-rich green tea extract (GTE) protects against nonalcoholic steatohepatitis (NASH) by alleviating gut-derived endotoxin translocation and hepatic Toll-like receptor-4 (TLR4)–nuclear factor κB (NFκB) inflammation. We hypothesized that intact GTE would attenuate NASH-associated responses along the gut–liver axis to a greater extent than purified (−)-epigallocatechin gallate (EGCG) or (+)-catechin (CAT). Male C57BL/6J mice were fed a low-fat diet, a high-fat (HF) diet, or the HF diet with 2% GTE, 0.3% EGCG or 0.3% CAT for 8 weeks prior to assessing NASH relative to endotoxemia, hepatic and intestinal inflammation, intestinal tight junction proteins (TJPs) and gut microbial ecology. GTE prevented HF-induced obesity to a greater extent than EGCG and CAT, whereas GTE and EGCG more favorably attenuated insulin resistance. GTE, EGCG and CAT similarly attenuated serum alanine aminotransferase and serum endotoxin, but only GTE and EGCG fully alleviated HF-induced NASH. However, hepatic TLR4/NFκB inflammatory responses that were otherwise increased in HF mice were similarly attenuated by GTE, EGCG and CAT. Each treatment also similarly prevented the HF-induced loss in expression of intestinal TJPs and hypoxia inducible factor-1α and the otherwise increased levels of ileal and colonic TNFα mRNA and fecal calprotectin protein concentrations. Gut microbial diversity that was otherwise lowered in HF mice was maintained by GTE and CAT only. Further, microbial metabolic functions were more similar between GTE and CAT. Collectively, GTE catechins similarly protect against endotoxin–TLR4–NFκB inflammation in NASH, but EGCG and CAT exert differential prebiotic and antimicrobial activities suggesting that catechin-mediated shifts in microbiota composition are not entirely responsible for their benefits along the gut–liver axis.

Intestinal-level anti-inflammatory bioactivities of catechin-rich green tea: Rationale, design, and methods of a double-blind, randomized, placebo-controlled crossover trial in metabolic syndrome and healthy adults

Metabolic endotoxemia initiates low-grade chronic inflammation in metabolic syndrome (MetS) and provokes the progression towards more advanced cardiometabolic disorders. Our recent works in obese rodent models demonstrate that catechin-rich green tea extract (GTE) improves gut barrier integrity to alleviate the translocation of gut-derived endotoxin and its consequent pro-inflammatory responses mediated through Toll-like receptor-4/nuclear factor κB (TLR4/NFκB) signaling. The objective of this clinical trial is to establish the efficacy of GTE to alleviate metabolic endotoxemia-associated inflammation in persons with MetS by improving gut barrier function. We plan a double-blind, placebo-controlled cross-over trial in persons with MetS and age- and gender-matched healthy persons (18–65 y; n = 20/group) who will receive a low-energy GTE-rich (1 g/day; 890 mg total catechins) confection snack food while following a low-polyphenol diet for 28 days. Assessments will include measures of circulating endotoxin (primary outcome) and secondary outcomes including biomarkers of endotoxin exposure, region-specific measures of intestinal permeability, gut microbiota composition, diversity, and functions, intestinal and systemic inflammatory responses, and catechins and microbiota-derived catechin metabolites. Study outcomes will provide the first report of the GTE-mediated benefits that alleviate gut barrier dysfunction in relation to endotoxemia-associated inflammation in MetS persons. This is expected to help establish an effective dietary strategy to mitigate the growing burden of MetS that currently affects ~35% of Americans.

Green Tea Extract Treatment in Obese Mice with Nonalcoholic Steatohepatitis Restores the Hepatic Metabolome in Association with Limiting Endotoxemia-TLR4-NFκB-Mediated Inflammation.

Catechin-rich green tea extract (GTE) alleviates nonalcoholic steatohepatitis (NASH) by lowering endotoxin-TLR4 (Toll-like receptor-4)-NFκB (nuclear factor kappa-B) inflammation. This study aimed to define altered MS-metabolomic responses during high-fat (HF)-induced NASH that are restored by GTE utilizing livers from an earlier study in which GTE decreased endotoxin-TLR4-NFκB liver injury. Mice are fed a low-fat (LF) or HF diet for 12 weeks and then randomized to LF or HF diets containing 0% or 2% GTE for an additional 8 weeks. Global MS-based metabolomics and targeted metabolite profiling of catechins/catechin metabolites are evaluated. GTE in HF mice restores hepatic metabolites implicated in dyslipidemia insulin resistance, and inflammation. These include 122 metabolites: amino acids, lipids, nucleotides, vitamins, bile acids, flavonoids, xenobiotics, and carbohydrates. Hepatic amino acids, B-vitamins, and bile acids are inversely correlated with biomarkers of insulin resistance, liver injury, steatosis, and inflammation. Further, phosphatidylcholine metabolites are positively correlated with biomarkers of liver injury and NFκB inflammation. Thirteen catechin metabolites are identified in livers of GTE-treated mice, mostly as phase II conjugates of parental catechins or microbial-derived valerolactones. The defined anti-inflammatory/metabolic interactions advance an understanding of the mechanism by which GTE catechins protect against NFκB-mediated liver injury in NASH.

Green Tea Extract (Camellia sinensis) as a Potential Antitumoral Agent on Breast Cancer Cells (FS13-04-19)

ObjectivesWe aimed to obtain a catechin-rich green tea extract (GTE) from Camellia sinensis and to evaluate its antitumor potential on human breast cancer. Green tea (GT) has been extensively studied for its antioxidant property, which is mainly attributed to catechins. These phenolic compounds regulate many cellular targets involved in cancer signaling pathways, including those mediated by p53 tumor suppressor protein. MethodsTea infusion was prepared on a ratio of 1 g:40 mL of boiling distilled water using a combination of temperature and time (70, 75, 80, 85, 90, 95 and 100 °C/5, 10, 15 min). Infusions were evaluated by polyphenols content (Folin–Ciocalteu’s reagent) and antioxidant potential (FRAP). Breast cancer cells (MDA-MB-231 and MCF-7) and non-tumoral cells (MCF-10A), were exposed to different concentrations of GTE (31.5 μg/mL to 1.0 mg/mL) during 24 h-48 h, and cell viability was assessed by Alamar Blue® and Trypan Blue assays. Viability was also acessed in the presence of a p53 protein inibitor, pifithrin-α. Immunocytochemistry and Western blotting analysis were performed to access the expression of p53. ResultsOur results demonstrated no influence of extraction condition in the total content of polyphenols and antioxidant potential of GT, and a new extract was obtained at 80 °C/5 min, then freeze dried to be used in cell culture. After exposure for 24 h, GTE already promoted a cytotoxic effect, reducing viability of both breast cancer cell lines (IC50 MDA-MB-231 = 138,8 μg/mL; IC50 MCF-7 = 324,5 μg/mL) without cytotoxic effect on non-tumoral cells (IC50 MCF-10A = 10,097 μg/mL). In addition, GTE promotes an increase of p53 levels on treated MCF-7 cells, which express the wild-type form of the protein. Interestingly, an opposite phenomenon was evidenced in MDA-MB-231 cells, that express the mutated form of p53, in which protein levels seem to be lower in the presence of the extract. ConclusionsOur data suggests that GTE has anticarcinogenic potential on breast cancer and it is possible that this capacity might be related with the modulation of p53 tumor suppressor protein. Funding SourcesFAPERJ, FUNDAÇÃO DO CÂNCER, CAPES, CNPq.

Effects of Catechin-rich Green Tea Extract on the MMP-1 Activity of HaCaT Keratinocyte Cells and on UVB-induced Skin Damage in Hairless Mice

Background: Skin is an organ that protects the human body from various environmental stimuli that can induce immune system activation. Skin aging can be largely divided into two categories: physiological aging, which is caused by the a decreased physiological function of the skin and structural changes with aging, and photoaging, which is caused by the chemical stress induced by external stimuli such as ultraviolet (UV) radiation.BR Methods and Results: The objective of this study was to investigate the anti-wrinkle and UV protective effect of catechin-rich green tea extract (CGTE) in activated keratinocyte (HaCaT cells) and UV-induced skin damage in hairless mice. The results showed that CGTE inhibits the tumor necrosis factor-alpha interferon-gamma (TNF-α + IFN-γ)-induced expression of matrix metalloproteinase (MMP)-1 in HaCaT cells. In addition, the CGTE treatment significantly reduced wrinkle formation, epidermal thickness, collagen deposition, and transepidermal water loss in dorsal skin irradiated with UVB. However, the β-glucosidase activity was significantly increased. The CGTE treatment inhibits mRNA expression and enzyme activity of MMP-2 and MMP-9 in the dorsal skin irradiated with UVB.BR Conclusions: It is expected that CGTE can be effectively used as a functional food and cosmetic ingredient to improve skin moisture retention and reduce wrinkle formation.

Green tea extract prevents obesity in male mice by alleviating gut dysbiosis in association with improved intestinal barrier function that limits endotoxin translocation and adipose inflammation

Gut-derived endotoxin translocation provokes obesity by inducing TLR4/NFκB inflammation. We hypothesized that catechin-rich green tea extract (GTE) would protect against obesity-associated TLR4/NFκB inflammation by alleviating gut dysbiosis and limiting endotoxin translocation. Male C57BL/6J mice were fed a low-fat (LF) or high-fat (HF) diet containing 0% or 2% GTE for 8 weeks. At Week 7, fluorescein isothiocyanate (FITC)-dextran was administered by oral gavage before assessing its serum concentrations as a gut permeability marker. HF-feeding increased (P<.05) adipose mass and adipose expression of genes involved in TLR4/NFκB-dependent inflammation and macrophage activation. GTE attenuated HF-induced obesity and pro-inflammatory gene expression. GTE in HF mice decreased serum FITC-dextran, and attenuated portal vein and circulating endotoxin concentrations. GTE in HF mice also prevented HF-induced decreases in the expression of intestinal tight junction proteins (TJPs) and hypoxia inducible factor-1α while preventing increases in TLR4/NFκB-dependent inflammatory genes. Gut microbial diversity was increased, and the Firmicutes:Bacteroidetes ratio was decreased, in HF mice fed GTE compared with HF controls. GTE in LF mice did not attenuate adiposity but decreased endotoxin and favorably altered several gut bacterial populations. Serum FITC-dextran was correlated with portal vein endotoxin (P<.001; rP=0.66) and inversely correlated with colonic mRNA levels of TJPs (P<.05; rP=−0.38 to −0.48). Colonic TJPs mRNA were inversely correlated with portal endotoxin (P<.05; rP=−0.33 to −0.39). These data suggest that GTE protects against diet-induced obesity consistent with a mechanism involving the gut-adipose axis that limits endotoxin translocation and consequent adipose TLR4/NFκB inflammation by improving gut barrier function.

Green tea extract inhibits early oncogenic responses in mice with nonalcoholic steatohepatitis.

Nonalcoholic steatohepatitis (NASH) increases hepatocellular carcinoma (HCC) risk. We hypothesized that the hepatoprotective anti-inflammatory benefits of catechin-rich green tea extract (GTE) would protect against HCC progression by inhibiting NASH-associated liver injury and pro-oncogenic responses. We used an HCC model in high-fat (HF)-fed mice that mimics early oncogenic events during NASH without inducing tumorigenesis and premature mortality. Male C57BL/6J mice (4-weeks old) were fed a HF diet containing GTE at 0% or 2%. Mice were administered saline or diethylnitrosamine (DEN; 60 mg kg-1, i.p.) at 5-weeks and 7-weeks of age. NASH, inflammation, fibrosis, and oncogenic responses were assessed at 25-weeks of age. Saline-treated mice showed prominent histopathological signs of steatosis and hepatocellular ballooning. Although DEN did not impact adiposity, steatosis, ballooning and hepatic lipid accumulation, these parameters were attenuated by GTE regardless of DEN. Hepatic lipid peroxidation and fibrosis that were increased by DEN were attenuated by GTE. Hepatic TLR4, MCP1 and TNFα mRNA levels were unaffected by DEN, whereas iNOS was increased by DEN. These transcripts were lowered by GTE. GTE attenuated the frequency of PCNA+ hepatocytes and mRNA expression of cyclin D1, MIB1 and Ki-67 that were otherwise increased by DEN. GTE increase APAF1 mRNA that was otherwise lowered by DEN. Relative to saline-treated mice, DEN increased mRNA levels of oncostatin M, gp130, c-Fos, c-Myc and survivin; each was lowered by GTE in DEN-treated mice. These findings indicate that GTE may protect against hepatic oncogenesis by limiting early steps in the carcinogenic cascade related to NASH-associated HCC.

Catechin-rich green tea extract increases the expression of genes of the cholesterol synthetic pathways in livers of normal diet- and high-fat diet-fed rats

Background In vivo studies using rodents have shown that green tea extract (GT) and catechins isolated from green tea can induce a variety of health effects, including antiobesity, hypoglycemic and hypolipidemic activities. However, we and others observed that serum cholesterol levels were increased by GT and tea catechins in rats and mice [1]. In this study, we examined whether dietary GT affects the expression of genes involved in cholesterol synthesis. Materials and methods Catechin-rich (30% catechin) GT was used for the in vivo studies. Male Sprague-Dawley rats (average weight 237.7 g) were divided into six groups. The first group was fed a normal diet (ND, 10% calories from fat); the second group a high-fat diet (HFD, 40% calories from fat); the third group a ND containing 1% GT (ND + 1% GT); the fourth group a HFD + 1% GT; the fifth group a ND + 3% GT; and the sixth group a HFD + 3% GT. After 4 weeks of feeding, rats were euthanized by whole blood collection under anesthesia. Serum metabolites were determined using a dry chemistry analyzer. Total RNA samples extracted from the liver were used for microarray and quantitative real-time PCR (qPCR) analyses. Hepatic lipids were extracted with chloroform-methanol 2:1, and liver triglyceride (TG) and cholesterol (Cho) levels were determined. Results As reported previously, GT increased the serum levels of total cholesterol (T-Cho) and high-density lipoprotein cholesterol (HDL-Cho) in a concentration-dependent manner in both ND- and HFD-fed rats. Conversely, GT lowered hepatic TG and T-cho levels. Microarray analysis data suggested that GT increased more than two-fold the mRNA expression of nine hepatic genes involved in cholesterol synthesis out of 21 analyzed in ND-fed rats. qPCR analysis revealed that GT significantly increased the mRNA levels of six genes involved in cholesterol synthesis in ND-fed rats. Similar but smaller effects of GT also were observed in HFD-fed rats. Conclusions The results suggested that GT increased serum cholesterol levels, at least in part, through the increased expression of genes in the cholesterol synthetic pathways in the liver. GT also increased the mRNA levels of Srebf2 and Insig1, which are positively regulated by SREBP2. Therefore, dietary GT may increase expression of these genes by SREBP2 activation.

Catechin-rich green tea extract increases serum cholesterol levels in normal diet- and high fat diet-fed rats

Background In vivo studies using rodents have shown that green tea extract and catechins isolated from green tea can induce a variety of health effects, including anti-obesity, hypoglycemic and hypolipidemic activities [1]. These beneficial effects of green tea have been observed in experiments using high fat, high cholesterol and high fructose diet-fed animals. In the present study, we examined the effects of catechinrich green tea extract on serum glucose and lipid levels in normal diet-and high fat diet-fed rats.

Total Phenolic Content, Antioxidant Activity, and Cross-Cultural Consumer Rejection Threshold in White and Red Wines Functionally Enhanced with Catechin-Rich Extracts

White and red wines spiked with catechin-rich green tea extract and grape seed extract were assessed for phenolic content, antioxidant activity, and cross-cultural consumer rejection thresholds in relation to wine as a functional food. Health functionality is an important factor in functional foods, and spiking pure compounds or plant extracts is an effective method to increase or control functionality. The total phenolic content and antioxidant activity were measured in wines spiked to different extract concentrations, namely, control and 50, 100, 200, 400, and 800 mg/L, to confirm the dose-response curves in both white and red wines. Consumer rejection thresholds (CRTs) were established for spiked wines in a Korean and in an Australian population. Our results showed that the green tea extract and grape seed extract increased the antioxidant activity dose dependently, and the CRTs varied considerably between the Korean and the Australian groups, with Koreans preferring wines spiked with green tea extract and Australians showing a preference for wines spiked with grape seed extract. These results have implications for producing wine products that are enhanced in phenolic compounds and targeted to different cultural groups.

Green tea extract improves running endurance in mice by stimulating lipid utilization during exercise

A series of polyphenols known as catechins are abundant in green tea, which is consumed mainly in Asian countries. The effects of catechin-rich green tea extract (GTE) on running endurance and energy metabolism during exercise in BALB/c mice were investigated. Mice were divided into four groups: nonexercise control, exercise control (Ex-cont), exercise+0.2% GTE, and exercise+0.5% GTE groups. Treadmill running time to exhaustion, plasma biochemical parameters, skeletal muscle glycogen content, beta-oxidation activity, and malonyl-CoA content immediately after exercise were measured at 8-10 wk after the initiation of the experiment. Oxygen consumption and respiratory exchange ratio were measured using indirect calorimetry. Running times to exhaustion in mice fed 0.5% GTE were 30% higher than in Ex-cont mice and were accompanied by a lower respiratory exchange ratio, higher muscle beta-oxidation activity, and lower malonyl-CoA content. In addition, muscle glycogen content was high in the GTE group compared with the Ex-cont group. Plasma lactate concentrations in mice fed GTE were significantly lower after exercise, concomitant with an increase in free fatty acid concentrations. Catechins, which are the main constituents of GTE, did not show significant effects on peroxisome proliferator-activated receptor-alpha or delta-dependent luciferase activities. These results suggest that the endurance-improving effects of GTE were mediated, at least partly, by increased metabolic capacity and utilization of fatty acid as a source of energy in skeletal muscle during exercise.