Tea Catechin Suppresses Adipocyte Differentiation Accompanied by Down-regulation of PPARγ2 and C/EBPα in 3T3-L1 Cells

Furuyashiki, Takashi; Nagayasu, Hironobu; Aoki, Yukiko; Bessho, Hiroaki; Hashimoto, Takashi; Kanazawa, Kazuki; Ashida, Hitoshi

doi:10.1271/bbb.68.2353

Cited by 241 publications

(187 citation statements)

References 34 publications

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“…EGCG inhibits proliferation and adipose differentiation of the 3T3-L1 preadipocyte cell line, and induces apoptosis in 3T3-L1 adipocytes (11)(12)(13). Pure EGCG and green tea extracts have both been shown in humans to stimulate brown fat thermogenesis (14,15).…”

Section: Epigallocatechin-3-gallate (Egcg)mentioning

confidence: 99%

Epigallocatechin-3-gallate (EGCG), A Green Tea Polyphenol, Suppresses Hepatic Gluconeogenesis through 5′-AMP-activated Protein Kinase

Collins

Liu

et al. 2007

Journal of Biological Chemistry

306

224

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Epigallocatechin-3-gallate (EGCG), a main catechin of green tea, has been suggested to inhibit hepatic gluconeogenesis. However, the exact role and related mechanism have not been established. In this study, we examined the role of EGCG in hepatic gluconeogenesis at concentrations that are reachable by ingestion of pure EGCG or green tea, and are not toxic to hepatocytes. Our results show in isolated hepatocytes that EGCG at relatively low concentrations (<1 M) inhibited glucose production via gluconeogenesis and expression of key gluconeogenic genes. EGCG was not toxic at these concentrations while demonstrating significant cytotoxicity at 10 M and higher concentrations. EGCG at 1 M or lower concentrations effective in suppressing hepatic gluconeogenesis did not activate the insulin signaling pathway, but activated 5-AMP-activated protein kinase (AMPK). The EGCG suppression of hepatic gluconeogenesis was prevented by blockade of AMPK activity. In defining the mechanism by which EGCG activates AMPK, we found that the EGCG activation of AMPK was mediated by the Ca 2؉ /calmodulin-dependent protein kinase kinase (CaMKK). Furthermore, our results show that the EGCG activation of AMPK and EGCG suppression of hepatic gluconeogenesis were both dependent on production of reactive oxygen species (ROS), which was a known activator of CaMKK. Together, our results demonstrate an inhibitory role for EGCG in hepatic gluconeogenesis and shed new light on the mechanism by which EGCG suppresses gluconeogenesis.

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Section: Epigallocatechin-3-gallate (Egcg)mentioning

confidence: 99%

Epigallocatechin-3-gallate (EGCG), A Green Tea Polyphenol, Suppresses Hepatic Gluconeogenesis through 5′-AMP-activated Protein Kinase

Collins

Liu

et al. 2007

Journal of Biological Chemistry

306

224

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“…Obesity is a condition in which adipocytes accumulate a large amount of fat and become enlarged. It is characterized at the cellular level by an increase in the number and size of adipocytes differentiated from fibroblastic preadipocytes in adipose tissue (3).…”

Section: Introductionmentioning

confidence: 99%

Effects of Flavonoids and Phenolic Acids on the Inhibition of Adipogenesis in 3T3-L1 Adipocytes

Hsu

Yen

2007

J. Agric. Food Chem.

222

174

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Obesity has become a global epidemic in both developed and developing countries, and it is a significant risk factor for various diseases such as diabetes, cancer, heart disease, and hypertension. In the present study, the effect of naturally occurring antioxidants (flavonoids and phenolic acids) on the inhibition of adipogenesis in 3T3-L1 adipocytes was investigated. The results showed that o-coumaric acid and rutin had the highest inhibition on intracellular triglyceride (61.3 and 83.0%, respectively) among 15 phenolic acids and 6 flavonoids tested. However, the oil red o stained material (OROSM) showed that cell number in 3T3-L1 adipocytes was not influenced by those compounds. For glycerol-3-phosphate dehydrogenase (GPDH) activity, the data indicated that o-coumaric acid and rutin had the highest inhibition on GPDH activity (54.2 and 66.8%, respectively) among the compounds tested. o-Coumaric acid and rutin also inhibited the expression of PPARγ, C/EBPR and leptin and then up-regulated expression of adiponectin at the protein level. Some naturally occurring antioxidants efficiently suppressed adipogenesis in 3T3-L1 adipocytes. These results suggest that o-coumaric acid and rutin targeted for adipocyte functions could be effective in improving the symptoms of metabolic syndrome.

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“…Epidemiological studies and experimental data show that drinking green tea or administration of its components, green tea catechins (GTCs), is associated with a lower risk of obesity [3][4][5][6][7][8][9][10]. Moreover, GTCs are involved in modulating fat metabolism [3,5,6,8,[11][12][13], but the mechanisms are not clear.…”

mentioning

confidence: 99%

Green tea catechins prevent obesity through modulation of peroxisome proliferator-activated receptors

Yan

Zhao

Bao

2013

Sci. China Life Sci.

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Epidemiological evidence and experimental studies suggest that drinking green tea is associated with a lower risk of obesity and related diseases. However, the mechanisms of these effects are not clear. In the present study, we investigated the antiobesity mechanisms of green tea catechins (GTCs) through modulation of peroxisome proliferator activated-receptor (PPAR) pathways in high-fat diet-induced obesity in rats. GTC supplementation significantly attenuated the increased body and liver weights and the elevated serum and liver triglyceride levels. Meanwhile, GTCs increased the PPARγ levels in subcutaneous white adipose tissue (SWAT) and decreased the PPAR levels in visceral white adipose tissue (VWAT). In addition, GTC treatment up-regulated the levels of PPARδ in SWAT, VWAT, and brown adipose tissue and increased the expression of genes involved in fatty acid oxidation in brown adipose tissue. Our results suggest that GTCs exert their anti-obesity mechanism in part by modulating PPAR signaling pathways. obesity, green tea catechins, peroxisome proliferator activated-receptors (PPARs), hyperlipidemia, metabolic syndrome

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Tea Catechin Suppresses Adipocyte Differentiation Accompanied by Down-regulation of PPARγ2 and C/EBPα in 3T3-L1 Cells

Cited by 241 publications

References 34 publications

Epigallocatechin-3-gallate (EGCG), A Green Tea Polyphenol, Suppresses Hepatic Gluconeogenesis through 5′-AMP-activated Protein Kinase

Epigallocatechin-3-gallate (EGCG), A Green Tea Polyphenol, Suppresses Hepatic Gluconeogenesis through 5′-AMP-activated Protein Kinase

Effects of Flavonoids and Phenolic Acids on the Inhibition of Adipogenesis in 3T3-L1 Adipocytes

Green tea catechins prevent obesity through modulation of peroxisome proliferator-activated receptors

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