Green tea supplementation ameliorates insulin resistance and increases glucose transporter IV content in a fructose-fed rat model

Wu, Liang; Juan, Chi Chang; Hwang, Lucy Sun; Hsu, Yung Pei; Ho, Pei Hsuan; Ho, Low Tone

doi:10.1007/s00394-004-0450-x

Cited by 182 publications

(115 citation statements)

References 32 publications

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“…Accordingly, the doses (5-100 M) of EGCG (the effective dose of this study is in the range of 20 -100 M) or other tea catechins generally used in this study that are compatible with the goal of helping to regulate the initiation and progression of obesity and diabetes (27) were a little bit higher, but might be acceptable for the physiological effect of EGCG in animals. This is indirectly supported by the evidence that green tea extract given to rats by oral administration at a dosage of 0.5 g/100 ml water, which contained ϳ2,183 M EGCG, could within 12 wk improve insulin sensitivity in rats and that green tea extract containing 327 M EGCG enhanced glucose uptake in rat adipocytes in vitro (53).…”

Section: Discussionsupporting

confidence: 56%

Inhibitory effect of green tea (−)-epigallocatechin gallate on resistin gene expression in 3T3-L1 adipocytes depends on the ERK pathway

Liu

Chen

Hung

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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is known as an adipocyte-specific secretory hormone that can cause insulin resistance and decrease adipocyte differentiation. By contrast, green tea catechins, especially (Ϫ)-epigallocatechin gallate (EGCG), have been reported as body weight and diabetes chemopreventatives. Whether EGCG regulates production of Rstn is unknown. Using 3T3-L1 adipocytes, we found that EGCG at 20 and 100 M suppressed Rstn mRNA levels by ϳ35 and 50%, respectively, after 3 h. The basal half-life of Rstn mRNA induced by actinomycin D was Ͼ12 h but shifted to 3 h in the presence of EGCG. This suggests that EGCG regulates the stability of Rstn mRNA. Treatment with cycloheximide did not prevent EGCGsuppressed Rstn mRNA levels, which suggests that the effect of EGCG does not require new protein synthesis. Intracellular Rstn protein significantly decreased in the presence of 100 M EGCG 3 h after treatment, whereas the release of the Rstn protein did not significantly change. This suggests that EGCG may modulate the distribution of Rstn protein between the intracellular and extracellular compartments. EGCG did not affect the amounts of extracellular signal-related kinase-1/2 (ERK1/2), phospho-JNK, phospho-p38, and phospho-Akt proteins but reduced the amounts of phospho-ERK1/2 proteins. Overexpression with MEK1 blocked EGCG-inhibited Rstn mRNA expression. These data suggest that EGCG downregulates Rstn expression via a pathway that is dependent on the ERK pathway.genistein; mitogen-activated protein kinase; extracellular signal-related kinase RESISTIN (RSTN) IS A CYSTEINE-RICH POLYPEPTIDE HORMONE (20,38) that, depending on the species, contains 4 -5 exons, 3-4 introns, 575-1217 bp of mRNA, and 108 -114 amino acids of protein (10 -12.5 kDa) (16,23,44,45). Rstn is first isolated from adipose tissues and found to link obesity to type 2 diabetes (44). In particular, Rstn mRNA expression in adipose tissues of obese humans is higher than that in normal subjects (12). In addition, a single nucleotide polymorphism in the Rstn gene promoter is associated with obesity (14) and diabetes (35), and the plasma Rstn levels are elevated in patients with obesity (12) and type 2 diabetes (59). Moreover, the dominant negative form of Rstn enhances adipogenesis and improves insulin sensitivity (24). Ever since its discovery, Rstn also has been found to possess numerous other actions. For example, Rstn regulates fasted blood glucose (6), causes dyslipidemia (39), suppresses insulin-stimulated glucose uptake in adipocytes (44) and muscle cells (30), inhibits dopamine and norepinephrine release in the hypothalamus (8), and promotes endothelial cell activation (50) and smooth muscle proliferation (9). To our knowledge, the expression of Rstn gene can be regulated by nutritional, endocrine, genetic, pharmacological, and developmental factors (5), and the mechanisms of action of Rstn are emerging. For example, Rstn promotes smooth muscle cell proliferation through the activation of extracellular signalregulated kinase (ERK1/2) and phosphatidylinositol 3-kinase (PI3K) ...

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Section: Discussionsupporting

confidence: 56%

Inhibitory effect of green tea (−)-epigallocatechin gallate on resistin gene expression in 3T3-L1 adipocytes depends on the ERK pathway

Liu

Chen

Hung

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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“…Although (Ϫ)-catechin displays different effects on the regulation of adiponectin expression from the major green tea polyphenols, it would be worthwhile in a further in vivo study to explore whether the effect of (Ϫ)-catechin on adiponectin gene expression in our in vitro study is related to the mechanism by which green tea extracts exert their antidiabetic (26) and antiobesity (16) actions in animals.…”

Section: Discussionmentioning

confidence: 99%

(−)-Catechin suppresses expression of Kruppel-like factor 7 and increases expression and secretion of adiponectin protein in 3T3-L1 cells

Cho

Park²,

Shin³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

105

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Adiponectin is an adipocyte-specific secretory hormone that can increase insulin sensitivity and promote adipocyte differentiation. Administration of adiponectin to obese or diabetic mice reduces plasma glucose and free fatty acid levels. Green tea polyphenols possess many pharmacological activities such as antioxidant, anti-inflammatory, antiobesity, and antidiabetic activities. To investigate whether green tea polyphenols have an effect on the regulation of adiponectin, we measured expression and secretion levels of adiponectin protein after treatment of each green tea polyphenols in 3T3-L1 adipocytes. We found that (−)-catechin enhanced the expression and secretion of adiponectin protein in a dose- and time-dependent manner. Furthermore, treatment of (−)-catechin increased insulin-dependent glucose uptake in differentiated adipocytes and augmented the expression of adipogenic marker genes, including PPARγ, CEBPα, FAS, and SCD-1, when (−)-catechin was treated during adipocyte differentiation. In search of the molecular mechanism responsible for inducible effect of (−)-catechin on adiponectin expression, we found that (−)-catechin markedly suppresses the expression of Kruppel-like factor 7 (KLF7) protein, which has recently been reported to inhibit the expression of adiponectin and other adipogenesis related genes, including leptin, PPARγ, C/EBPα, and aP2 in adipocytes. KLF7 is a transcription factor in adipocyte and plays an important role in the pathogenesis of type 2 diabetes. Taken together, these data suggest that the upregulation of adiponectin protein by (−)-catechin may involve, at least in part, suppression of KLF7 in 3T3-L1 cells.

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“…They also found that daily supplementation of 0.5 g of green tea for 12 weeks could reduce fasting plasma glucose levels, insulin, triglyceride, and free fatty acids in Sprague-Dawley rats. 49,50 Islam et al reported that green tea intake of 23 g per day could increase serum insulin concentration in rats, and higher consumption of green tea can be beneficial for normal human subjects with hyperlipidemia. 51 Therefore, certain doses of green tea were beneficial for diabetes prevention.…”

Section: Discussionmentioning

confidence: 99%

Tea Consumption and Risk of Type 2 Diabetes: A Meta-Analysis of Cohort Studies

Jing

Han

et al. 2009

J GEN INTERN MED

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BACKGROUND: Tea consumption has been extensively studied in relation to various diseases, several epidemiologic studies have been performed to investigate the association of tea consumption with type 2 diabetes; however, the results of these studies were not entirely consistent. OBJECTIVE:To conduct a meta-analysis of studies that assessed the association of tea consumption and the risk of type 2 diabetes. RESEARCH DESIGN AND METHODS:We performed a systematic literature search through November 2008 in PUBMED, MEDLINE, EMBASE, and Cochrane Database of Systematic Reviews. The search was limited to Englishlanguage studies. Studies were excluded if they were type 1 diabetes, animal studies. Nine cohort studies were identified by two authors, and summary relative risks (RRs) were calculated using a random-effects model. RESULTS:We identified nine cohort studies, including 324,141 participants and 11,400 incident cases of type 2 diabetes with follow-up ranging from 5 to 18 years. The summary adjusted RR did not show that tea consumption was associated with a reduced type 2 diabetes risk (RR, 0.96; 95% confidence interval (CI), 0.92-1.01). Evidence from the results of our stratified analyses revealed that tea consumption ≥4 cups per day (RR, 0.8; 95% CI, 0.7-0.93) might play a role in the prevention of type 2 diabetes. However, no statistically significant association was observed for sex and the follow-up durations stratified between tea consumption and type 2 diabetes. CONCLUSIONS:This meta-analysis indicates that tea consumption ≥4 cups per day may lower the risk of type 2 diabetes.KEY WORDS: type 2 diabetes; tea; meta-analysis.

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Green tea supplementation ameliorates insulin resistance and increases glucose transporter IV content in a fructose-fed rat model

Abstract: Based on these results, we suggest that the amelioration of insulin resistance by green tea is associated with the increased expression of GLUT IV.

Cited by 182 publications

References 32 publications

Inhibitory effect of green tea (−)-epigallocatechin gallate on resistin gene expression in 3T3-L1 adipocytes depends on the ERK pathway

Inhibitory effect of green tea (−)-epigallocatechin gallate on resistin gene expression in 3T3-L1 adipocytes depends on the ERK pathway

(−)-Catechin suppresses expression of Kruppel-like factor 7 and increases expression and secretion of adiponectin protein in 3T3-L1 cells

Tea Consumption and Risk of Type 2 Diabetes: A Meta-Analysis of Cohort Studies

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