Epigallocatechin-3-Gallate Reduces Visceral Adiposity Partly through the Regulation of Beclin1-Dependent Autophagy in White Adipose Tissues

Abstract

Epigallocatechin-3-gallate (EGCG) is a primary bioactive phytochemical in green tea. Its therapeutic potential in metabolic diseases has been reported; however, the molecular mechanisms of the anti-obesity effect of EGCG have not been fully elucidated. In this study, we examined the effects of EGCG on lipid metabolism and autophagy in adipose tissue. After 8 weeks of high-fat diet feeding, mice were treated with EGCG (20 mg/kg/day) for 2 weeks to test in vivo anti-obesity effects of EGCG. EGCG treatment improved glucose tolerance and caused body weight loss. Interestingly, reduced adipose tissue mass was more prominent in visceral compared to subcutaneous white adipose tissue. Mechanistically, EGCG treatment increased autophagic flux in white adipose tissue through the AMP-activated protein kinase-mediated signaling pathway. Adipocyte-specific knockout of Beclin1 mitigated the effects of EGCG on visceral adipose tissue mass and glucose tolerance, indicating that the anti-obesity effect of EGCG requires Beclin1-dependent autophagy. Collectively, our data demonstrated that EGCG has anti-obesity effects through the upregulation of Beclin1-dependent autophagy and lipid catabolism in white adipose tissue (WAT).

Epigallocatechin-3-Gallate Dampens Non-Alcoholic Fatty Liver by Modulating Liver Function, Lipid Profile and Macrophage Polarization

“…Similarly, the liver weight and the liver/body weight ratio of the EGCG-25 and EGCG-50 groups were dramatically decreased in comparison to the PBS group. Indeed, the beneficial impact of EGCG on body weight and liver weight in NAFLD has been observed in previous studies of EGCG treatment of murine NAFLD [ 27 , 28 , 29 ].…”

“…To place our studies in the context of previous work done in this field, we compared our findings with those reported in the literature [ 27 , 28 , 29 , 31 , 33 , 40 , 41 , 42 , 43 , 44 , 45 , 46 ]. There is ample evidence in the literature that EGCG attenuates obesity [ 28 , 40 ], insulin resistance [ 33 ] and fatty liver disease [ 41 ] in rodents fed a high-fat diet by increasing activity of mitochondrial respiratory chain complexes [ 42 ], suppressing hepatic cholesterol synthesis [ 43 ], decreasing bile acid and lipid absorption [ 44 ], and modulating the interaction between gut microbiota and bile acids [ 45 , 46 ].…”

Therapeutic Effects of Catechins in Less Common Neurological and Neurodegenerative Disorders

“…This amelioration was due to the restoration of autophagic flux, decrease of apoptotic cells, and reduction of soluble and insoluble Aβ1–42 levels in the hippocampal CA1 region of stressed rats [ 45 ]. Catechins increase the amount of available Beclin-1 [ 46 ], a protein that regulates endocytosis and autophagy. Catechins also exert neuroprotective effects through the protein kinase C (PKC) signaling cascade [ 47 ], reducing the levels of apoptotic markers such as Bad, Bax, caspase-3, and poly(ADP-ribose) polymerase (PARP) [ 48 ].…”

Dietary Polyphenols in Metabolic and Neurodegenerative Diseases: Molecular Targets in Autophagy and Biological Effects

“…Apart from resveratrol, other polyphenolic compounds with protective effects through autophagy activation in obesity have been assessed. A treatment with epigallocatechin-3-gallate (EGCG) for two weeks in a mice model of high-fat diet (HFD)-induced obesity stimulated both autophagic flux in white adipose tissue in an AMPK-dependent manner and beclin-1 activation [107]. Very interestingly, the effect of a 30 days' supplementation with resveratrol on gene expression and adipose tissue morphology in a cohort of obese men has been reported.…”