Share this article Share with email Share with twitter Share with linkedin Share with facebook. Abstract 1. Oxidative stress is recognized as a major contributing factor for the development of late complications of diabetes. Tea contains polyphenolic compounds catechins , which have many important biological properties, including strong anti-oxidant activity.

The present study was undertaken to evaluate the effect of tea catechins epigallocatechin gallate EGCG , epigallocatechin EGC , epicatechin gallate ECG and epicatechin EC on markers of oxidative stress malondialdehyde MDA , reduced glutathione GSH and membrane -SH group in erythrocytes from type 2 diabetics.

Oxidative stress was induced in normal and type 2 diabetic erythrocytes by incubating with tert-butyl hydroperoxide t-BHP. Diabetic erythrocytes have higher MDA and decreased GSH and membrane -SH groups compared with normal erythrocytes.

Our results show that tea catechins protect erythrocytes from t-BHP-induced oxidative stress, the effect being more pronounced in diabetic erythrocytes. We hypothesise that a higher intake of catechin-rich food by diabetic patients may provide some protection against the development of long-term complications of diabetes.

References Articles referenced by this article 45 Title not supplied AUTHOR UNKNOWN. Title not supplied Ramachandran Relation between insulin resistance and plasma concentrations of lipid hydroperoxides, carotenoids, and tocopherols.

Facchini FS , Humphreys MH , DoNascimento CA , Abbasi F , Reaven GM Am J Clin Nutr, 3 MED: Role of oxidative stress in development of complications in diabetes. Baynes JW Diabetes, 4 MED: Oxygen free radicals and iron in relation to biology and medicine: some problems and concepts.

Halliwell B , Gutteridge JM Arch Biochem Biophys, 2 MED: Maridonneau I , Braquet P , Garay RP J Biol Chem, 5 MED: UE 2,4-diaminopyrrolopyrimidine , a potent inhibitor of membrane lipid peroxidation as assessed by the production of 4-hydroxynonenal, malondialdehyde, and 4-hydroxynonenal--protein adducts.

Rohn TT , Nelson LK , Waeg G , Quinn MT Biochem Pharmacol, 10 MED: Oxidative protein damage in plasma of type 2 diabetic patients. Telci A , Cakatay U , Kayali R , Erdogan C , Orhan Y , Sivas A , Akcay T Horm Metab Res, 1 MED: Oxygen radicals stimulate intracellular proteolysis and lipid peroxidation by independent mechanisms in erythrocytes.

Davies KJ , Goldberg AL J Biol Chem, 17 MED: Increased plasma oxidizability and decreased erythrocyte and plasma antioxidative capacity in patients with NIDDM.

Zaltzberg H , Kanter Y , Aviram M , Levy Y Isr Med Assoc J, 4 MED: Show 10 more references 10 of Smart citations by scite.

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Explore citation contexts and check if this article has been supported or disputed. Polyphenol Supplementation and Antioxidant Status in Athletes: A Narrative Review. Bojarczuk A , Dzitkowska-Zabielska M Nutrients , 15 1 , 29 Dec Cited by: 3 articles PMID: PMCID: PMC Review Articles in the Open Access Subset are available under a Creative Commons license.

Flavonoid and Phenolic Acid Profiles of Dehulled and Whole Vigna subterranea L. Verdc Seeds Commonly Consumed in South Africa. Okafor JNC , Meyer M , Le Roes-Hill M , Jideani VA Molecules , 27 16 , 18 Aug Cited by: 0 articles PMID: PMCID: PMC Articles in the Open Access Subset are available under a Creative Commons license.

Erythrocyte Deformability and Na,K-ATPase Activity in Various Pathophysiological Situations and Their Protection by Selected Nutritional Antioxidants in Humans.

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Preclinical and Clinical Antioxidant Effects of Natural Compounds against Oxidative Stress-Induced Epigenetic Instability in Tumor Cells. Bouyahya A , El Menyiy N , Oumeslakht L , El Allam A , Balahbib A , Rauf A , Muhammad N , Kuznetsova E , Derkho M , Thiruvengadam M , Shariati MA , El Omari N Antioxidants Basel , 10 10 , 29 Sep Cited by: 11 articles PMID: PMCID: PMC Review Articles in the Open Access Subset are available under a Creative Commons license.

The Emerging Role of Polyphenols in the Management of Type 2 Diabetes. Wang Y , Alkhalidy H , Liu D Molecules , 26 3 , 29 Jan Cited by: 19 articles PMID: PMCID: PMC Review Articles in the Open Access Subset are available under a Creative Commons license. Similar Articles To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation.

Protective role of tea catechins on erythrocytes subjected to oxidative stress during human aging. Maurya PK , Rizvi SI Nat Prod Res , 23 12 , 01 Jan Cited by: 36 articles PMID: Rizvi SI , Zaid MA Clin Chim Acta , , 24 Dec Cited by: 21 articles PMID: Intracellular reduced glutathione content in normal and type 2 diabetic erythrocytes: effect of insulin and - epicatechin.

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Red Wine Numerous studies have investigated the relationship between consumption of red wine and susceptibility to certain chronic diseases including lung cancer, prostate cancer, and cardiovascular disease.

Cardiovascular disease: Consumption of red wine has been associated with a reduction in endothelin-1 a molecule involved in blood pressure regulation , a reduction in myocardial ischemic reperfusion injury an injury to the heart when blood is returned to the organ after a period of restriction , increased HDL concentrations, decreased platelet aggregation clumping , increased fibrinolysis breakdown of a clot , and increased plasma antioxidant activity 4,5.

Furthermore, results from some studies indicate that consumption of red wine may slow the progression of atherosclerosis. Diabetes Mellitus: The flavanols in red wine may improve the lipid profile in some individuals.

Insulin sensitivity and reduced insulin resistance has been reported to improve in individuals with moderate wine consumption 5.

In animal studies, increased HDL lipoproteins, lowered levels of ox-LDL, decreased platelet aggregation and improvements in endothelial function have been reported following moderate red wine consumption 6.

In a randomized study conducted on individuals with controlled Type II Diabetes, the catechins in the red wine were reported t significantly increase plasma HDL levels by 2.

Lung Cancer: Research studies have focused on the correlation of COPD Chronic Obstructive Pulmonary Disease and increased lung cancer risk. Consistent with its putative antioxidant abilities, moderate consumption of red wine has been associated with a reduced risk of lung cancer in comparison to individuals who do not consume red wine 8.

Prostate Cancer: There have been contradicting results regarding consumption of red wine and cancer. Results from some studies suggest that consumption of red wine over a lifetime posed increased risks of prostate cancer.

Further research is needed to better understand the amount and time period of red wine consumption and the associated risks to prostate cancer 9. Conclusions: In light of this research, the American Heart Association does not recommend consumption of alcohol to reduce risk of cardiovascular disease and the American Cancer Society recommends limiting consumption of alcoholic beverages.

If adults choose to drink alcoholic beverages, the Dietary Guidelines for Americans, recommends they do so in moderation. Moderation is considered 1 drink defined as 12 ounces of beer, 5 ounces of wine, 1.

FIGURE 1. Timeline of in vivo experiments. Rabbits were randomized into six groups. Group 1 Control : control rabbits given saline intragastrically after injured carotid artery operation.

Group 2 DM : diabetic rabbits given saline intragastrically after injured carotid artery operation. Group 4 DM-sham : injured carotid artery of diabetic rabbits washed and then incubated 10 min by saline after injured operation. Group5 DM-EPC : autologous L-EPCs transplanted into the area of injured carotid artery of diabetic rabbits after injured carotid artery operation.

Group 6 DM-EGCG-EPC : EGCG pre-treated autologous L-EPCs transplanted into the area of injured carotid artery of diabetic rabbits after injured carotid artery operation.

The diabetic rabbits were then given normal diet for 4—6 weeks with fasting blood glucose level checked once per week. Rabbit carotid injury was performed by using a 3. Figure 1 shows the timeline of the in vivo experiment. After that, a total of 1 × 10 6 cells were resuspended in μl of 4°C saline.

Immediately after the balloon withdrawal, cells were injected into the carotid lumen, and were kept for 10 min before the incision was closed. The pictures were taken and the area of denudation was identified using the NIH Image J software by an investigator blinded to the group assignment.

In CM-Dil labeled L-EPC auto-transfusion groups, the homing of transplanted EPCs to the site of injured vascular was analyzed using fluorescent microscopy Olympus, Tokyo, Japan.

Then, cells were randomized into four groups: control, mannitol, high glucose, and high glucose group with EGCG 40 μM treatment. For the high glucose group, cells were co-incubated with 30 mM glucose, whereas cells in the osmotic pressure control mannitol group were co-incubated with 30 mM mannitol.

To detect the exact proliferation rates of L-EPCs an EDU 5-ethynyldeoxyuridine incorporation assay was executed with the Cell-Light TM EdU in vitro Imaging Kit Ribobio, Guangzhou, China according to the manufacturer instructions. After the EDU staining, cell nuclei were stained with Hoechst and observed with an inverted fluorescent microscope Olympus, Tokyo, Japan.

For each group, 6 random fields were photographed. The proliferation rate refers to the number of EDU stained cells divided by the number of Hoechst stained cells. Late endothelial progenitor cells migration assay was performed with a modified Boyden chamber assay as described previously Qiu et al.

Cells were examined under a fluorescent microscope Olympus, Tokyo, Japan at a × total magnification and 6 random fields were photographed for each sample. The average number of migrated cells in the 6 random fields was computed and used as the migration number for the group.

Total RNA of the cultured L-EPCs was extracted with standard TRIZOL Invitrogen, Carlsbad, CA, United States method. β-actin was used as endogenous controls for mRNAs expression. Primers of Akt, eNOS, and β-actin were synthetized by Invitrogen Carlsbad, CA, United States.

Cells in a 6-well plate were scraped in a RIPA lysis buffer Beyotime, Shanghai, China supplemented with 1 mM PMSF. After incubations in an enhanced chemiluminescence reagent Amersham, Haemek, Israel , images were captured and analyzed on the LAS image reader system Fujifilm, Tokyo, Japan.

Data were presented as means ± SEM. Analyses were conducted with SPSS A total of about 3 × 10 6 —1 × 10 7 of PBMCs was isolated from each 20 ml blood sample. Most of the cells were double-positive for Dil-acLDL uptake and FITC—lectin binding Figure 2B.

There were FIGURE 2. Identification of L-EPCs. A The panel shows the sequential changes of L-EPCs. All the pictures were taken under × magnification.

B The L-EPCs shows both Dil-uptaken red and lectin binding green ability × magnification. C Flow-cytometry reveals the L-EPCs expressed abundant CD34 and KDR molecule.

Numbers are presented as Mean ± SEM. Percentage of positive cells for all experiment is determined by comparison with corresponding negative control labeling. There was no statistical difference on rabbit weight and age among all the three groups data not shown.

Diabetic model was rendered successfully by using an alloxan method. The average fasting blood glucose level was 5. Compared with the control group, diabetic rabbits showed poor reendothelialization ratios after carotid injury FIGURE 3. Reendothelialization of injured carotid arteries is promoted by EGCG.

A Reendothelialization of injured carotid arteries is promoted by intragastrically-given of EGCG. The blue area, which was rendered by Evans Blue, represent the area of carotid artery where lack of endothelium. The control group shows the best reendothelialization, whereas diabetes rabbits show very poor reendothelialization.

After intragastrically given EGCG for 7 days, the reendothelialization rates risen. The number of rabbits in each group was 6. DM: diabetic rabbits were given with saline intragastrically after injured carotid artery operation.

B EGCG pre-treated autologous L-EPCs transfusion improved diabetic rabbits carotid reendothelialization. DM-sham: injured carotid artery of diabetic rabbits were washed and then incubated 10 min by saline after injured operation.

DM-EPC: autologous L-EPCs were transplanted into the area of injured carotid artery of diabetic rabbits after injured carotid artery operation.

DM-EGCG-EPC: EGCG pre-treated autologous L-EPCs were transplanted into the area of injured carotid artery of diabetic rabbits after injured carotid artery operation. C Representative figure of autologous L-EPC tracking in vivo under fluorescent microscope.

Picture shows the extent to which L-EPCs are involved in reendothelialization 7 days after carotid artery injury. CM-DiI-labeled L-EPCs red are attached to endothelium FITC-lectin-stained, green. Nuclei of L-EPC were stained with DAPI blue. To identify whether EGCG benefits carotid reendothelialization through improving the functions of L-EPCs, we transfused autologous L-EPCs to the carotid injured rabbits.

Compared with diabetic sham-operated group, diabetic autologous L-EPCs transplantation locally to the injured carotid artery showed an accelerated trend of the reendothelialization process, but statistical difference was not found After EGCG pre-treatment for 72 h, autologous L-EPCs transfusion strongly improved the reendothelialization of diabetic rabbits Moreover, autologous L-EPCs transfusion group EGCG pre-treated displayed clearly more CM-Dil labeled L-EPCs attached to the endothelium, compared with the non-pre-treated ECGG group Figure 3C.

Late endothelial progenitor cells viability was determined by a CCK-8 test. We first examined the toxicity of EGCG to L-EPCs. Total confluent L-EPCs cultured in well plate were added different concentrations of EGCG and their absorbance at nm was examined.

As shown in Figure 4A , up to 40 μM concentration of EGCG showed no poisonousness to L-EPCs. The typical IC50 of EGCG is μM. High glucose treatment for 72 h directly impaired the proliferation of L-EPCs, while this impairment was greatly blocked in a time-and-dose dependent manner by EGCG.

EGCG treatment of 40 μM for 72 h could most effectively recover the proliferation of L-EPCs impaired by high glucose Figures 4B,C. FIGURE 4. EGCG improves L-EPCs proliferation and migration under high glucose condition.

A CCK-8 test reveals that up to 40 μM EGCG shows no poisonousness to L-EPCs, the typical IC50 of the chemical is μM.

B,C L-EPCs incubated in high glucose environment 30 mM were co-incubated under different concentrations of EGCG 1—40 μM for different time 24—72 h. Histogram reveals that high glucose treatment for 72 h directly impairs the proliferation of L-EPCs, this impairment could be block by EGCG in a time and dose dependent manner.

D EDU incorporation assay × magnification. The magnification is × The mobility of L-EPCs was examined by a Boyden chamber assay. The mRNA level of both Akt and eNOS remained unmodified by 72 h high glucose treatment. Also the EGCG treatment did not affect the Akt and eNOS mRNA level Figure 5A.

Compared with the control group, high glucose blocked the phosphorylation of Akt and eNOS in diabetic rabbits by half as shown in the western blot test, and the EGCG treatment restored the level of p-Akt and p-eNOS completely Figures 5B,C.

FIGURE 5. EGCG re-activates Akt-eNOS pathway blocked by high glucose treatment. A RT-PCR shows the relative expression of Akt and eNOS mRNA, which were not changed significantly between the different groups.

B,C Western blot reveals the phosphorylation of Akt and eNOS were blocked by HG treating, and recovered by 40 μM EGCG co-incubation for 72 h.

The primary cause of vascular complications in diabetes mellitus is hyperglycaemia, associated with endothelial dysfunction and impaired neovascularisation. Clinical studies have revealed that diabetic patients usually have both low numbers and low activities of EPCs Fadini et al. In diabetic patients, L-EPCs, which have more important effect than early-EPCs during repair of artery injury, exhibit impaired abilities of differentiation, proliferation, adhesion and migration, tubulisation, secretion, mobilization, and homing Chen et al.

Other studies have reported that high glucose condition, similar to diabetes mellitus, could directly suppress the proliferation, migration and Akt activity of L-EPCs Nakamura et al. Epigallocatechin gallate is known as an antioxidant, but recent investigations have revealed other direct actions independent from it, such as anti-hypertrophy, anti-inflammatory, anti-myocardial infarction and anti-atherosclerosis Kim et al.

In one study Wu et al. Our previous studies show, neonatal rat cardiomyocytes and human endothelial cells are cultured with 40 μM EGCG treatment for 24 h Yu et al.

In this study, six different EGCG concentrations from 10 to μM and three different durations 24, 48, and 72 h are tested. Among those, 40 μM EGCG treatment for 72 h displays the optimal improvement on the proliferation and migration of L-EPCs.

Here, we first observed that EGCG could improve reendothelialization of injured carotid artery of diabetic rabbits. To find out whether L-EPCs is involved, subsequent EGCG pre-treated L-EPCs autotransfusion experiments were performed.

We find that the EGCG 40 μM for 72 h pre-treated L-EPCs show significantly improved maturation of endothelial cells than L-EPCs only, consequently ameliorate reendothelialization of the injured artery in diabetic rabbits.

To find out the underlined mechanism, the mobility and proliferation of L-EPCs are examined. Finally, our study shows that EGCG improves the reendothelialization of diabetic rabbits, potentially by promoting the proliferation and migration of L-EPCs under high glucose condition.

Several signal pathways have been reported to play important roles under high glucose condition induced suppression of EPCs Dimmeler et al. However, this pathway is suppressed under high glucose condition Chen et al. However, the exact mechanism of how EGCG promotes the phosphorylation of Akt and eNOS need to be investigated in future studies.

Study from Conti and the group about human endothelial cells also confirms that the pathway of Sirt1 is a critical regulator of oxidative stress response and cellular lifespan Conti et al. And other investigation proves phytochemicals may act as positive modulators of neuroinflammatory events Corbi et al.

Therefore, EGCG might have acted on multiple pathways to improve endothelial function and the whole anti-oxidative environment, which contribute to increased reendothelialization in diabetic rabbits.

But, to our knowledge, present study is the first one showing that EGCG improves the reendothelialization of carotid artery in diabetic rabbits, potentially by promoting the proliferation and migration of L-EPCs under the high glucose condition. The activations of the phosphorylation of Akt and eNOS play an important role during this process.

What is noteworthy is that concentrations used in our in vivo study are supramaximal to average daily tea consumption. Data displayed that when human average daily tea consumption almost contains mg EGCG, the maximum blood concentration is 7. The maximum blood concentration is Therefore, our experimental results should not be made an analogy to the real world simply.

In conclusion, our study demonstrates the efficacy of EGCG on endothelial dysfunction in carotid artery caused by diabetics, and the potential of EGCG in treating diabetic peripheral atherosclerotic disease in clinical application.

HH and DH designed and performed the study. HH, C-yJ, and DH wrote the manuscript with input from all authors. C-yJ, X-kB, and LY designed and performed the animal experiments. S-jX, Y-bZ, and M-hW performed the cell growth and in vivo studies. C-yJ and Y-xS performed the analytic calculations and statistical analysis.

All authors provided critical feedback and helped to shape the research, analysis, and manuscript. The present study was supported by National Natural Science Foundation of China Nos.

LY16H and LY17H , and Medical and Health Research Project of Zhejiang Province, China No. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. We are grateful to the Biomedical Research Center in Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University for the technical support.

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Sensitivity analyses were used to evaluate the stability of the results by removing a single study each time to identify the effect of individual studies on the pooled effect size. Meta-regression analysis was performed to examine the association between the net change in fasting glucose, fasting insulin or HbA 1c and intervention dose, treatment duration, intervention type, caffeine content, different ethnicity or study design.

The search strategy identified abstracts. After the titles and abstracts were screened, articles were excluded and 95 articles underwent full-text review. A further 68 articles were excluded for the following reasons: 26 articles did not provide relevant outcomes, 14 articles involved green tea as a multicomponent supplement in the experimental group, 12 articles were excluded because the subjects had been treated with black tea or oolong tea.

Finally, 27 eligible articles met the inclusion criteria and were included in the meta-analysis Fig. Table 1. Of the 27 trials with 28 comparisons included in the current meta-analysis, 13 comparisons [ 22 , 23 , 24 , 25 , 28 , 29 , 30 , 33 , 36 , 39 , 46 , 48 ] were conducted in western countries and 15 comparisons [ 26 , 27 , 31 , 32 , 34 , 35 , 37 , 38 , 40 , 41 , 42 , 43 , 44 , 45 , 47 ] were conducted in Asian countries.

Twenty comparisons [ 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 33 , 36 , 38 , 39 , 41 , 42 , 45 , 46 , 47 , 48 ] were performed in subjects with normal FBG and 8 comparisons [ 31 , 32 , 34 , 35 , 37 , 40 , 43 , 44 ] were performed in subjects with high level FBG.

Most comparisons 25 of 28 used a parallel study design [ 22 , 23 , 24 , 26 , 27 , 28 , 29 , 30 , 31 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 45 , 46 , 47 , 48 ], while others 3 comparisons used a crossover design [ 25 , 32 , 44 ].

Twelve comparisons [ 22 , 24 , 25 , 27 , 29 , 33 , 35 , 37 , 38 , 39 , 48 ] adjusted for the confounding effect of caffeine on glucose and insulin, 13 comparisons [ 26 , 28 , 30 , 31 , 32 , 34 , 36 , 40 , 41 , 42 , 43 , 44 , 45 ] used caffeinated green tea, and 3 [ 23 , 46 , 47 ] did not report the use of coffee.

Twenty comparisons [ 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 46 , 47 , 48 ] used green tea extract capsule and eight comparisons [ 22 , 31 , 32 , 41 , 42 , 43 , 44 , 45 ] used green tea beverage Table 1. The study quality of the 27 included RCTs varied.

Most trials did not report details regarding allocation concealment 14 of 27 [ 26 , 28 , 30 , 31 , 32 , 36 , 37 , 40 , 41 , 42 , 43 , 44 , 46 , 48 ] or randomization method 15 of 27 [ 23 , 28 , 30 , 31 , 32 , 33 , 36 , 37 , 40 , 41 , 42 , 43 , 44 , 45 , 48 ]. Twenty-two trials used double-blinded design [ 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 45 , 46 , 47 , 48 ], one trial used a single-blinded design [ 22 ], and four trials used an open-label design [ 31 , 32 , 33 , 44 ].

Three trials did not report the dropout rate or the reasons for the dropouts [ 28 , 40 , 44 ] Table 2. Primary outcome measures included changes in FBG, FBI, and HbA 1c.

Meta-analysis of the effects of green tea on fasting blood glucose concentrations. Meta-analysis of the effects of green tea on fasting blood insulin concentrations.

Meta-analysis of the effects of green tea on HbA lc concentrations. Secondary outcome measures included changes in HOMA-IR concentration.

Green tea supplementation had no significant effect on HOMA-IR WMD: In the subgroup analysis, green tea consumption significantly lowered FBG concentrations in subjects using green tea capsule or with high catechins dosage, subjects from western countries, subjects in short duration of green tea supplementation, subjects with normal FBG, studies with caffeinated green tea intake, studies with parallel design, and studies with low quality.

However, significant reduction in fasting glucose was not found in other subgroups. In addition, the beneficial effect for green tea supplementation on fasting insulin was observed in subjects with green tea capsule, subjects from western countries, subjects with normal baseline FBG and studies with decaffeinated green tea intake.

However, no effect was found in other subgroups. Significant reductions in HbA 1c concentrations were observed in subjects from Asian countries, studies with caffeine in green tea and studies with low quality, while the obvious effect was not found in other subgroups Table 3.

Meta-regression found no linear relations between WMD in FBG, FBI or HbA 1C and intervention dose Fig. Furthermore, meta-regression found no linear relations between WMD in FBG or FBI and treatment duration, caffeine content, different ethnicity, intervention type and study design.

a Relation between the WMD of FBG and intervention dose in 27 independent randomized controlled comparisons. b Relation between the WMD of FBI and intervention dose in 18 independent randomized controlled comparisons.

c Relation between the WMD of HbA lc and intervention dose in 11 independent randomized controlled comparisons. Each circle represents a study, telescoped by its weight in the analysis. The funnel plots of the studies were symmetrical for fasting glucose, fasting insulin, and HbA 1c Supplementary Figure 1.

A sensitivity analysis was performed to confirm the robustness of our findings. The result was consistent after removing each trial for both fasting glucose and fasting insulin. In the sensitivity analysis of HbA 1c , the exclusion of one trial [ 22 ] Basu resulted in significant reductions of However, there was no significant reduction in HbA 1c after the removal of other trials.

This meta-analysis involving 27 RCTs with subjects evaluated the effect of green tea supplementation on glycemic control. We found that green tea supplementation significantly reduced FBG concentration, while the effect of green tea on other glycemic variables such as FBI, HbA 1c , and HOMA-IR was not significant.

Our results are consistent with some previous meta-analysis [ 49 , 50 ], which also showed that green tea consumption resulted in a significant reduction in FBG. While, another previous meta-analysis [ 8 ] suggested that green tea consumption had favorable effects on decreasing both FBG and HbA 1c concentrations.

In our study, we did not find a significant improvement in HbA 1c concentrations. Observational prospective cohorts and case-control studies have been performed to determine the effect of green tea supplementation on glycemic control, although the results are conflicting. Some RCTs also found beneficial effects on glycemic control, including reducing fasting glucose and fasting insulin [ 38 , 48 ].

In contrast, several RCTs have reported no significant correlations between green tea intake and glycemic control [ 24 , 27 ]. Nonetheless, these results need to be interpreted with caution because the number of patients enrolled in most trials was too limited, at less than patients; in addition, the intervention duration and catechins dosages were varied among studies.

So, more RCTs with larger subjects and longer duration were needed to find out the real relationship between green tea consumption and blood glucose control. Recent mechanistic studies have examined the effects of green tea consumption on glucose control and provided further evidence for the biological plausibility of these findings.

Green tea may affect glucose control through different mechanisms. First, tea catechins have been reported to reduce carbohydrate absorption from the intestine via inhibition of intestinal sucrose, alpha-amylase, and alpha-glucosidase [ 10 ].

Second, Tea catechins might also inhibit the hepatic gluconeogenesis through regulation of the expression of gluconeogenic genes and protein-tyrosine phosphorylation in the mouse liver [ 52 ]. Third, tea catechins could enhance insulin sensitivity and glucose metabolism there by helping to prevent the development of T2DM [ 53 ].

Furthermore, Tea catechins are also powerful antioxidants that can ameliorate oxidative stress [ 54 ]. In this meta-analysis, subgroup analyses were performed based on predefined variables to identify potential sources of heterogeneity.

Green tea consumption significantly decreased FBG and FBI only in subjects using green tea capsule. In addition, meta-regression also pointed out that green tea capsule was associated with HbA 1C.

Nowadays, there was still insufficient evidence on whether green tea capsule was more biologically active compared to green tea beverage in vivo or vitro studies. In addition, subgroup analyses revealed that green tea with caffeine had a more pronounced effect on FBG and HbA 1C than the decaffeination subgroup.

As tea naturally contains caffeine in addition to catechins and other compounds, whether caffeine intake influences the glucose control of tea remains controversial [ 55 , 56 ].

As there were a limited number of subjects in the subgroup analysis, these results may not be generalized. Our study had several strengths. First, we only selected RCTs in this meta-analysis, which ensured a relatively high-quality and provided reliable inference about causality.

Second, both parallel and crossover studies were included in this meta-analysis. Crossover trials are generally considered to have a more-robust design than parallel trials because of reduced intraparticipant variability.

We considered it important to include all these studies because they represented a comprehensive evidence for our analysis. Third, results were less likely to be influenced by publication bias.

Furthermore, subgroup analyses were undertaken to detect potential sources of heterogeneity for primary outcomes. Our study also had several limitations. HbA 1c is an important indicator for glucose control, including greater pre-analytical stability, greater convenience, and less day-to-day perturbations.

In addition, it also takes a number of months to detect delayed effects of green tea on insulin resistance. In addition, we could not ascertain the safety margin in this meta-analysis because no serious side effects were reported in the included trials.

However, mild side effects such as mild skin rashes, gastric disturbances, and abdominal bloating were reported in some clinical studies [ 57 ]. Third, the size of these trials, which ranged between 25 and participants, were indeed limited.

Therefore, our meta-analysis may have been underpowered to detect a true effect. Forth, the quality of RCTs included in this meta-analysis varied. Some of the RCTs did not provide detailed randomization process.

Of the 27 trials, almost half of the trials were of high risk of bias, which may also affect the reliability of our findings.

In conclusion, green tea intake had a favorable effect on fasting blood glucose concentration. However, green tea intake did not significantly affect fasting blood insulin or HbA 1c.

In future, high-quality larger RCTs with long-term follow-up are needed to investigate the effect of green tea supplementation on glycemic control, especially the long-term effects on fasting insulin and HbA 1c.

Pittas AG, Dawson-Hughes B, Sheehan P, Ware JH, Knowler WC, Aroda VR, Brodsky I, Ceglia L, Chadha C, Chatterjee R, Desouza C, Dolor R, Foreyt J, Fuss P, Ghazi A, Hsia DS, Johnson KC, Kashyap SR, Kim S, LeBlanc ES, Lewis MR, Liao E, Neff LM, Nelson J, O'Neil P, Park J, Peters A, Phillips LS, Pratley R, Raskin P, Rasouli N, Robbins D, Rosen C, Vickery EM, Staten M, Group DdR.

Vitamin D supplementation and prevention of type 2 diabetes. N Engl J Med. Article CAS PubMed PubMed Central Google Scholar. Cho NH, Shaw JE, Karuranga S, Huang Y, da Rocha Fernandes JD, Ohlrogge AW, Malanda B.

IDF diabetes atlas: global estimates of diabetes prevalence for and projections for Diabetes Res Clin Pract. Article CAS PubMed Google Scholar. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, Nathan DM.

Diabetes prevention program research G: reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. Lotfy M, Adeghate J, Kalasz H, Singh J, Adeghate E. Chronic complications of diabetes mellitus: a mini review.

Curr Diabetes Rev. Hou LQ, Liu YH, Zhang YY. Garlic intake lowers fasting blood glucose: meta-analysis of randomized controlled trials. Asia Pac J Clin Nutr. CAS PubMed Google Scholar. Balentine DA, Wiseman SA, Bouwens LC. The chemistry of tea flavonoids.

Crit Rev Food Sci Nutr. Khan N, Mukhtar H. Tea polyphenols for health promotion. Life Sci. Liu K, Zhou R, Wang B, Chen K, Shi LY, Zhu JD, Mi MT.

Effect of green tea on glucose control and insulin sensitivity: a meta-analysis of 17 randomized controlled trials. Am J Clin Nutr. Jing Y, Han G, Hu Y, Bi Y, Li L, Zhu D. Tea consumption and risk of type 2 diabetes: a meta-analysis of cohort studies. J Gen Intern Med.

Article PubMed PubMed Central Google Scholar. Collins QF, Liu HY, Pi J, Liu Z, Quon MJ, Cao W. J Biol Chem. Wu LY, Juan CC, Hwang LS, Hsu YP, Ho PH, Ho LT. Green tea supplementation ameliorates insulin resistance and increases glucose transporter IV content in a fructose-fed rat model.

Eur J Nutr. Belcaro G, Ledda A, Hu S, Cesarone MR, Feragalli B, Dugall M. Greenselect phytosome for borderline metabolic syndrome. Evid Based Complement Alternat Med. PubMed PubMed Central Google Scholar. Igarashi Y, Obara T, Ishikuro M, Matsubara H, Shigihara M, Metoki H, Kikuya M, Sameshima Y, Tachibana H, Maeda-Yamamoto M, Kuriyama S.

Randomized controlled trial of the effects of consumption of 'Yabukita' or 'Benifuuki' encapsulated tea-powder on low-density lipoprotein cholesterol level and body weight. Food Nutr Res. Article PubMed PubMed Central CAS Google Scholar.

Josic J, Olsson AT, Wickeberg J, Lindstedt S, Hlebowicz J. Does green tea affect postprandial glucose, insulin and satiety in healthy subjects: a randomized controlled trial.

Nutr J. Stroup DF, Berlin JA, Morton SC, Olkin I, Williamson GD, Rennie D, Moher D, Becker BJ, Sipe TA, Thacker SB. Meta-analysis of observational studies in epidemiology: a proposal for reporting. Meta-analysis of observational studies in epidemiology MOOSE group. Moher D, Pham B, Jones A, Cook DJ, Jadad AR, Moher M, Tugwell P, Klassen TP.

Does quality of reports of randomised trials affect estimates of intervention efficacy reported in meta-analyses? Anzures-Cabrera J, Sarpatwari A, Higgins JP. Expressing findings from meta-analyses of continuous outcomes in terms of risks. Stat Med. Article PubMed Google Scholar.

Follmann D, Elliott P, Suh I, Cutler J. The differences may be due to the fact that they used EGCG solution without toting up any additive. However, in the present case drinks were prepared by adding flavor and artificial sweetener that may be a reason for improved consumption.

The current results showing reduced body weight gain in groups consuming drinks containing catechins or EGCG are in consistent with the study of Basu et al. Inhibited lipid absorption from meals might be other reason for reduced weight gain [ 18 ].

Results for decreased cholesterol and LDL levels are in consistent with the work of Kim et al. Hypocholesterolemic potential of catechins can be accredited to increased fecal excretion of cholesterol and bile acid [ 20 ]. Tea catechins increase the bile acid excretion by preventing reabsorption from small intestine through disruption of micelle formation of bile acid.

This increased excretion of bile acid and cholesterol activates cholesterol 7α-hydroxylase that enhances the conversion of liver cholesterol to bile acid to restock this loss thus resulting in cholesterol reduction.

This decrease in hepatic cholesterol content in turn stimulates LDL receptor expression and lowers blood cholesterol level [ 21 ].

Results for non-significant effect of drinks on HDL are in agreement with previous work of Gomikawa et al. The effects could be due to presence of various bioactive components present in green tea [ 4 ].

Roghani and Baluchnejadmojarad [ 23 ] noted LDL reduction in diabetic rat modeling with EGCG. The proposed mechanism of LDL reduction by green tea catechins is through inhibition of cholesterol synthesis and dietary cholesterol absorption [ 24 ].

Crude catechins decrease plasma cholesterol concentrations by upregulating LDL receptor. The increase in the LDL receptor improves the uptake of low density lipoprotein cholesterol from the blood circulation [ 25 ].

Moreover, reduced expression of 3-hydroxymethylglutaryl coenzyme A reductase HMGR might be another reason for hypocholesterolemic activity of green tea as green tea EGCG also inhibits HMGR activity [ 26 , 27 ].

Low concentration of triglycerides by green tea might result from suppressed expression of stearoyl-CoA desaturase SCD 1 gene.

Because in liver triglyceride synthesis depends on the expression of the SCD 1 gene, that is involved in biosynthesis of oleate and palmitoleate, the major monounsaturated fatty acids of triglycerides. However, Watanabe et al. Reduced glucose level by green tea is supported by the work of Polychronopoulos et al.

The antihyperglycemic effect of green tea may be due to activated uptake of glucose, inhibited intestinal glucose transporter and decreased expression of gluconeogenesis controlling genes [ 30 ]. EGCG exhibits hypoglycemic potential by preventing the intestinal glucose absorption via sodium-dependent glucose transporter SGLT1 , lowering the expression of mRNA for gluconeogenesis controlling enzymes [ 31 ] and causing repression of glucose production, phosphoenolpyruvate carboxykinase PEPCK and glucosephosphatase gene expression, hepatocyte nuclear factor 1α HNF1α , and HNF4α in cells [ 32 ].

Additionally, EGCG has direct effect on hepatic glucose metabolism thus improving glucose stimulated insulin secretion [ 32 ].

Attenuation of insulin level with functional drinks in current exploration is supported by the work of Hsu et al. It is proposed that amelioration of insulin resistance by green tea is associated with increased expression of glucose transporter GLUT IV [ 34 ]. It can be concluded that green tea mitigates hypercholesterolemia and hyperglycemia effectually.

It has cholesterol lowering properties along with hypoinsulinemic capability that could be associated with improved insulin sensitivity. Our study demonstrates that drinks supplemented with catechins and EGCG are effective against obesity, hypercholesterolemia and hyperglycemia.

Consumption of functional drink reduced the body weight. Functional drinks resulted in significant reduction in body weight that could be caused by a decreased feed intake. Moreover, improvement in lipid profile was observed in all trials but more pronounced in semi-diseased states i.

trial-III and trial-II. Furthermore, serum glucose and insulin levels were also lowered significantly in the trial-III and IV. It was interesting to observe that catechins showed higher potency against hypercholesterolemia but EGCG reduced the hyperglycemia more effectively.

Devrim E, Erguder IB, Ozbek H, Durak I. High-cholesterol diet increases xanthine oxidase and decreases nitric oxide synthase activities in erythrocytes from rats. Nutr Res. Article CAS PubMed Google Scholar. Wu AH, Spicer D, Stanczyk FZ, Tseng CC, Yang CS, Pike MC.

Effect of 2-month controlled green tea intervention on lipoprotein cholesterol, glucose, and hormone levels in healthy postmenopausal women. Cancer Prev Res.

Article CAS Google Scholar. Butt MS, Ahmad RS, Sultan MT, Qayyum MMN, Naz A. Green tea and anticancer perspectives: Updates from last decade. Crit Rev Food Sci Nutr. Ahmad RS, Butt MS, Huma N, Sultan MT, Saeed F, Arshad MU, et al. Quantitative and qualitative portray of green tea catechins GTC through HPLC.

Int J Food Prop. Wolf BW, Weisbrode SE. Safety evaluation of an extract from Salaciaoblonga. Food Chem Toxicol. Stockbridge H, Hardy RI, Glueck CJ.

Photometric determination of cholesterol CHOD-PAP method. Ecoline® 2S, Merck KGaA, Darmstadt, Germany. J Lab Clin Med. CAS PubMed Google Scholar. McNamara JR, Cohn JS, Wilson PW, Schaefer EJ. Calculated values for low-density lipoprotein cholesterol in the assessment of lipid abnormalities and coronary disease risk.

Clin Chem. Annoni G, Botasso BM, Ciaci D, Donato MF, Tripodi A. Liquid triglycerides GPO-PAP. Lab J Res Lab Med. CAS Google Scholar. Thomas L, Labor U. Enzymateischer kinetischer colorimetrischer test GOD-PAP. Google Scholar. Besc W, Woltanski KP, Keilacker H, Diaz-Alonso JM, Schulz B, Amendt P, et al.

Measurement of insulin in human sera using a new RIA kit. Insulin determination in the absence of insulin antibodies—conventional assay and micro modification. Exp Clin I Endocrinol.

Article Google Scholar. Babu PVA, Sabitha KE, Shyamaladevi CS. Chemico Biol Interac. Yang MH, Wang CH, Chen HL. Green, oolong and black tea extracts modulate lipid metabolism in hyperlipidemia rats fed high-sucrose diet. J Nutr Biochem. Lee SM, Kim CW, Kim JK, Shin HJ, Baik JH. GCG-rich tea catechins are effective in lowering cholesterol and triglyceride concentrations in hyperlipidemic rats.

Basu A, Sanchez K, Leyva MJ, Wu M, Betts NM, Aston CE, et al. Green tea supplementation affects body weight, lipids, and lipid peroxidation in obese subjects with metabolic syndrome. J Am Coll Nutr. Byun JK, Yoon BY, Jhun JY, Oh HJ, Kim EK, Min JK, et al.

Immunol Lett. Choo JJ. Green tea reduces body fat aceration caused by high fat diet in rats through beta adrenocepter activation of thermogenesis in brown adipose tissue.

Wang S, Moustaid-Moussa N, Chen L, Mo H, Shastri A, Su R, et al. Novel insights of dietary polyphenols and obesity.

Article PubMed Central PubMed Google Scholar. Chen YK, Cheung C, Reuhl KR, Liu AB, Lee MJ, Lu YP, et al. J Agric Food Chem. Article PubMed Central CAS PubMed Google Scholar. Kim A, Chiu A, Barone MK, Avino D, Wang F, Coleman CI, et al.

Green tea catechins decrease total and low-density lipoprotein cholesterol: a systematic review and meta-analysis. J Am Diet Assoc. Yang TT, Koo MW. Chinese green tea lowers cholesterol level through an increase in fecal lipid excretion.

Life Sci. Goto T, Saito Y, Morikawa K, Kanamaru Y, Nagaoka S. Epigallocatechin gallate changes mRNA expression level of genes involved in cholesterol metabolism in hepatocytes.

Br J Nutr. Gomikawa S, Ishikawa Y, Hayase W, Haratake Y, Hirano N, Matuura H, et al. Effect of ground green tea drinking for 2 weeks on the susceptibility A of plasma and LDL to the oxidation ex vivo in healthy volunteers.

Kobe J Med Sci. Roghani M, Baluchnejadmojarad T. Hypoglycemic and hypolipidemic effect and antioxidant activity of chronic epigallocatechin-gallate in streptozotocin-diabetic rats.

Van Heek M, Farley C, Compton DS, Hoos L, Alton KB, Sybertz EJ, et al. Comparison of the activity and disposition of the novel cholesterol absorption inhibitor, SCH, and its glucuronide, SCH Br J Pharm.

Bursill CA, Abbey M, Roach PD. A green tea extract lowers plasma cholesterol by inhibiting cholesterol synthesis and upregulating the LDL receptor in the cholesterol-fed rabbit. Cuccioloni M, Mozzicafreddo M, Spina M, Tran CN, Falconi M, Eleuteri AM, et al.

Epigallocatechingallate potently inhibits the in vitro activity of hydroxymethyl-glutaryl-CoA reductase. J Lipid Res. examined the effects of exercise combined with dietary intervention on obese children and adolescents associated with the FTO -rs polymorphism. After 4 weeks of intervention, the levels of TC and LDL were significantly reduced in genotype AA or AT compared with genotype TT [ 23 ].

In addition, a clinical trial in obese subjects with the FTO -rs gene variant demonstrated that decreases in hs-CRP, TC and LDL levels were larger in A carriers during 3 months of low fat hypo-caloric diet [ 24 ].

In contrast, some studies did not report the role of FTO -rs polymorphism in response to interventions. Schum et al. studied the effects of FTO rs gene polymorphism on body composition and metabolism following a 6-month lifestyle intervention in overweight children.

FTO variant rs had no impact on BMI, body composition and metabolic profile insulin, HOMA, lipids, liver function tests before and after lifestyle intervention [ 25 ]. Different interventions, type and characteristics of study persons are potential reasons for discrepant findings.

This study showed that taking EGCG supplements for 2 months in patients T2DM was associated with a significant decrease in serum cholesterol level, but did not influence other lipid profiles TG, HDL and LDL. In addition, Zheng et al. in a meta-analysis observed that the consumption of beverages and extracts of green tea caused a decrease in serum concentrations of TC by 7.

Possible mechanisms by which EGCG decreases plasma cholesterol include: interfering with the micellar solubilization of cholesterol in the digestive tract and decreased absorption [ 20 ], enhanced biliary cholesterol secretion and attenuated liver cholesterol accumulation [ 28 ], induced up-regulation of LDL receptor in HepG2 cells [ 29 ].

In contrast to our results, a double-blind clinical trial studied the effect of decaffeinated green tea extract mg of EGCG on obese individuals with type 2 diabetes [ 30 ]. No significant differences were reported between the EGCG and placebo groups in FBS and lipid profile TG, Chol, HDL and LDL.

However, a significant reduction in WC, HbA 1c , insulin and HOMA-IR levels was reported after EGCG intervention compared to baseline [ 30 ]. Also, Mielgo-Ayuso et al. No significant difference was reported in the weight, fat mass, energy and fat metabolism, TG, cholesterol and LDL, or insulin resistance after EGCG intervention [ 31 ].

These discrepancies in results might be due to the different dosages, duration of the intervention, sample size, and clinical characteristics of the patients at baseline.

In our study, intervention of EGCG caused a significant reduction in DBP level. In the context, most previous studies were consistent with our results. A meta-analysis suggested that green tea consumption significantly decreased SBP —1. Furthermore, a meta-analysis thirteen studies reported that green tea and its catechins can improve blood pressure SBP, by —2.

In another study, Han et al. reported that EGCG inhibited caffeine-induced cardiovascular activity such as arterial pressure and heart rate [ 34 ]. Epigallocatechingallate reduces blood pressure through several mechanisms such as: maintaining vascular tone through balancing vasoconstricting and vasodilating substances [ 35 ], improving ventricular function and increasing nitric oxide production from endothelium [ 36 ] and reducing oxidative stress and managing the generation of ROS through inducing antioxidant enzymes and inhibiting pro-oxidant enzymes [ 37 ].

The present study is among the first clinical trials to investigate the effects of genotype-intervention interaction for the FTO -rs polymorphism on response to EGCG supplementation on metabolic and inflammatory changes in T2DM.

In conclusion, the results of this study show that intervention with EGCG supplements for 2 months in patients with T2DM had a significant improvement on BMI and DBP in A allele carriers of FTO -rs polymorphism, a high-risk group for T2DM; however, it did not affect inflammation and other lipid profiles.

This study suggests that administration of EGCG supplement may provide an advantageous therapy for patients with T2DM by using genome-customized approaches.

Current issue Archive Manuscripts accepted About the Journal Editorial office Editorial board Abstracting and indexing Subscription Contact Ethical standards and procedures Most read articles Instructions for authors Article Processing Charge APC Regulations of paying article processing charge APC.

Manuscripts accepted. About the Journal Editorial office Editorial board Abstracting and indexing Subscription Contact Ethical standards and procedures Most read articles.

Instructions for authors Article Processing Charge APC Regulations of paying article processing charge APC. Current issue. Effects of epigallocatechin gallate on total antioxidant capacity, biomarkers of systemic low-grade inflammation and metabolic risk factors in patients with type 2 diabetes mellitus: the role of FTO-rs polymorphism.

Seyedahmad Hosseini 1. Meysam Alipour 1. Mehrnoosh Zakerkish 2. Bahman Cheraghian 3. Pegah Ghandil 4. Nutrition and Metabolic Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Endocrinology and Metabolism, Health Research Institute, Diabetes Research Center, Jundishapur University of Medical Sciences, Ahvaz, Iran.

Department of Statistics and Epidemiology, Faculty of Public Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Medical Genetics, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Meysam Alipour. body mass index. Metabolic Syndrome. Introduction: Type 2 diabetes mellitus T2DM is known as one of the most common metabolic diseases and FTO polymorphism has been implicated in the susceptibility to this disease. Epigallocatechingallate EGCG has shown favorable effects on risk factors related to T2DM.

The present study aimed to investigate the effects of EGCG on total antioxidant capacity, biomarkers of systemic low-grade inflammation and metabolic risk factors in patients with T2DM considering the role of FTO polymorphism.

Material and methods: In this double-blind randomized clinical trial, 60 patients with T2DM 20—60 years were randomly allocated to three groups. Group 1 received mg of EGCG TT genotype. We genotyped FTO rs and measured body mass index BMI , blood pressure, profile lipid, interleukin-6, high sensitivity C-reactive protein and total antioxidant capacity, before and after the intervention, at 2 months.

Results: In carriers of A allele, EGCG intervention caused a significant decrease in BMI, diastolic blood pressure DBP , mean arterial pressure and serum cholesterol level compared with placebo p 0.

Conclusions: These findings suggest that carriers of the risk alleles A of FTO-rs have a better response to EGCG in improving BMI and DBP in patients with T2DM.

Introduction Type 2 diabetes mellitus T2DM is known as one of the most common metabolic diseases. Material and methods Participants Sixty-six patients with T2DM, screened from an endocrine clinic, were recruited.

Ethical approval The study was approved by the Ethics Committee of Ahvaz Jundishapur University of Medical Sciences ID: IR. Study design and randomization This study was a randomized double-blind placebo-controlled trial conducted in Ahvaz, Iran, from August to March Figure 1 Flowchart of the study.

Anthropometric and blood pressure measurement Weight accuracy of 0. Biochemical measurements The blood samples 5 ml were collected during the study 2 months in the hour fasting condition.

Genotyping A 5 ml blood sample was collected in EDTA containing tubes and stored at —80°C for extraction of DNA. Statistical analysis All analyses were performed with SPSS Results Of the volunteers, were eligible and underwent genotyping, anthropometric and biochemical assessments.

Table I Baseline characteristics of study patients. a Post-baseline changes within groups. Table II Effects of epigallocatechingallate EGCG on anthropometric indexes and blood pressure, regarding FTO -rs Table III Between-group analysis of epigallocatechingallate EGCG effects, regarding FTO -rs a Changes between the three groups.

c Significant changes in EGCG group TT compared to placebo. Discussion In the current study, we investigated the modulation of metabolic and inflammatory responses to EGCG supplementation by polymorphism of FTO -rs in patients with T2DM. Ogurtsova K , da Rocha , Huang Y , et al.

IDF Diabetes Atlas: global estimates for the prevalence of diabetes for and Diabetes Res Clin Pract. Google Scholar. Kanber EM , Ugurlucan M , Sahin M , Saribal D , Alpagut U. Do standard carotid artery endarterectomy and primary closure technique cause early restenosis in diabetic patients?

Arch Med Sci Atheroscler Dis. Nikolic D , Castellino G , Banach M , et al.