Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice

Santamarina, Aline Boveto; Carvalho-Silva, Milena; Gomes, Lara M.; Okuda, Marcos Hiromu; Santana, Aline Alves de; Streck, Emílio L.; Seelaender, Marília; Nascimento, Cláudia Maria Oller do; Ribeiro, Eliane; Lira, Fábio Santos; Oyama, Lila Missae

doi:10.1016/j.jnutbio.2015.07.002

Cited by 77 publications

(53 citation statements)

References 64 publications

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“…Importantly, studies have revealed that GrTPs act dose dependently, as high doses (0.4–0.8 mg/mL) activate apoptotic pathways through caspases and DNA breakdown to provoke anti-malignant effects [17]. Also, GrTPs promote weight loss in high doses (EGCG 1.3mg/g/daily [9], 3.2 mg/g every three days [51]) which can be beneficial for the regulation of hepatic enzymes (10–20 mg/g [54]) and metabolism (500 mg tablet/day [55]), as well as in metabolic syndrome and obesity (EGCG 0.05 mg/g [52]); yet, this is a side effect in certain situations where weight loss is not favored. In addition, GrTPs and EGCG in very high doses (3.2 mg/g) require further safety trials.…”

Section: Discussionmentioning

confidence: 99%

“…EGCG (0.05 mg/g/day) oral gavage regulated hepatic mitochondrial respiratory cascades and improved lipid metabolism, and insulin sensitivity in obese mice [52]. EGCG increased energy expenditure, and prevented oxidation of lipid substrates-stimulated by mitochondria and hepatic steatosis in this obesity model.…”

Section: Hepatic Complications and Green Tea Polyphenolsmentioning

confidence: 99%

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Chronic Inflammatory Diseases and Green Tea Polyphenols

2017

Nutrients

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Chronic inflammatory diseases affect millions of people globally and the incidence rate is on the rise. While inflammation contributes to the tissue healing process, chronic inflammation can lead to life-long debilitation and loss of tissue function and organ failure. Chronic inflammatory diseases include hepatic, gastrointestinal and neurodegenerative complications which can lead to malignancy. Despite the millennial advancements in diagnostic and therapeutic modalities, there remains no effective cure for patients who suffer from inflammatory diseases. Therefore, patients seek alternatives and complementary agents as adjunct therapies to relieve symptoms and possibly to prevent consequences of inflammation. It is well known that green tea polyphenols (GrTPs) are potent antioxidants with important roles in regulating vital signaling pathways. These comprise transcription nuclear factor-kappa B mediated I kappa B kinase complex pathways, programmed cell death pathways like caspases and B-cell lymphoma-2 and intervention with the surge of inflammatory markers like cytokines and production ofcyclooxygenase-2. This paper concisely reviews relevant investigations regarding protective effects of GrTPs and some reported adverse effects, as well as possible applications for GrTPs in the treatment of chronic and inflammatory complications.

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Section: Discussionmentioning

confidence: 99%

Section: Hepatic Complications and Green Tea Polyphenolsmentioning

confidence: 99%

Chronic Inflammatory Diseases and Green Tea Polyphenols

2017

Nutrients

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“…Important members of this subfamily include catechin, epicatechin, epigallocatechin, and the most biologically active one, epigallocatechin gallate (EGCG). Similar to other flavonoids, EGCG administered intraperitoneally or in the diet decreased body weight gain, visceral fat deposition, hyperglycemia, insulin resistance, liver functional enzymes, and hepatic steatosis following consumption of high‐fat diets (Santamarina et al, ). Decreased hepatic lipid accumulation may result from increased lipid oxidation through augmented electron transport chain activity.…”

Section: Treatment Of Non‐alcoholic Fatty Liver Diseasementioning

confidence: 98%

Non-alcoholic Fatty Liver Disease: Beneficial Effects of Flavonoids

Akhlaghi

2016

Phytother. Res.

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Non-alcoholic fatty liver disease (NAFLD) has been known as the hepatic feature of metabolic syndrome. Extra fat depots, especially in visceral areas, develop insulin resistance as a result of mild oxidation and inflammation. Insulin resistance induces lipolysis and releases free fatty acids into the circulation, where they are transported to the liver. In the liver, free fatty acids are converted to triglycerides and accumulate, causing simple steatosis that, if left untreated, can lead to steatohepatitis, and subsequently liver necrosis and cirrhosis.Flavonoids, a group of plant compounds with incredible biological characteristics, have shown advantages in pathological conditions. Beneficial effects of flavonoids against NAFLD and its related disorders have been observed in both animal and human studies. Various mechanisms have been found for their protection. Flavonoids prevent hepatosteatosis by increasing fatty acid oxidation in the liver. They can also reduce caloric intake and decrease body weight and fat deposition in visceral tissues. Flavonoids are unique antioxidants that exert their beneficial effects through inhibition of nuclear factor κB, thereby attenuating release of inflammatory cytokines, which are triggers of insulin resistance. Finally, flavonoids have shown to increase adiponectin, improve insulin sensitivity and glucose tolerance, correct dyslipidemia, and reduce blood pressure in patients with NAFLD. Copyright © 2016 John Wiley & Sons, Ltd.

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“…EGCG has multiple health benefits including the attenuation and prevention of liver fibrosis [16, 21, 22]. In vitro analysis shows that EGCG can abrogate liver fibrosis by inhibiting the proliferation of fibroblasts, reducing collagen deposition, and upregulating the mitochondrial respiratory chain [23]. Outside the spectrum of liver disease, EGCG can attenuate TGF-ß expression in pulmonary fibrosis [24].…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-Gallate Upregulates miR-221 to Inhibit Osteopontin-Dependent Hepatic Fibrosis

et al. 2016

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Osteopontin (OPN) promotes hepatic fibrosis, and developing therapies targeting OPN expression in settings of hepatic injury holds promise. The polyphenol epigallocatechin-3-gallate (EGCG), found in high concentrations in green tea, downregulates OPN expression through OPN mRNA degradation, but the mechanism is unknown. Previous work has shown that microRNAs can decrease OPN mRNA levels, and other studies have shown that EGCG modulates the expression of multiple microRNAs. In our study, we first demonstrated that OPN induces hepatic stellate cells to transform into an activated state. We then identified three microRNAs which target OPN mRNA: miR-181a, miR-10b, and miR-221. In vitro results show that EGCG upregulates all three microRNAs, and all three microRNAs are capable of down regulating OPN mRNA when administered alone. Interestingly, only miR-221 is necessary for EGCG-mediated OPN mRNA degradation and miR-221 inhibition reduces the effects of EGCG on cell function. In vivo experiments show that thioacetamide (TAA)-induced cell cytotoxicity upregulates OPN expression; treatment with EGCG blocks the effects of TAA. Furthermore, chronic treatment of EGCG in vivo upregulates all three microRNAs equally, suggesting that in more chronic treatment all three microRNAs are involved in modulating OPN expression. We conclude that in in vitro and in vivo models of TAA-induced hepatic fibrosis, EGCG inhibits OPN-dependent injury and fibrosis. EGCG works primarily by upregulating miR-221 to accelerate OPN degradation. EGCG may therefore have utility as a protective agent in settings of liver injury.

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Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice

Cited by 77 publications

References 64 publications

Chronic Inflammatory Diseases and Green Tea Polyphenols

Chronic Inflammatory Diseases and Green Tea Polyphenols

Non-alcoholic Fatty Liver Disease: Beneficial Effects of Flavonoids

Epigallocatechin-3-Gallate Upregulates miR-221 to Inhibit Osteopontin-Dependent Hepatic Fibrosis

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