Abstract
ABSTRACTBackground: A wealth of research has reported on the anti-obesity effects of green tea extract (GTE). Although browning of white adipose tissue (WAT) has been reported to attenuate obesity, no study has disclosed the effects of GTE on browning in Sprague Dawley rats.Objectives: The aims of the study were to investigate the effects of GTE on anti-obesity and browning, and their underlying mechanisms.Methods: Four groups of rats (n=10/group) were used including a normal diet with vehicle treatment, and a high-energy diet (HED) with vehicle or GTE by oral gavage at 77.5 or 155 mg/kg/day for 8 weeks. Body weight, fat accumulation, and serum biochemical parameters were used to evaluate obesity. The gene expressions were analyzed using RT-qPCR and western blotting.Results: GTE modulated HED-induced body weight, fat accumulation, and serum levels of triacylglycerol, total cholesterol, low-density lipoprotein, free fatty acids, aspartate aminotransferase, and alanine aminotransferase. Moreover, GTE enhanced the serum high-density lipoprotein. Most importantly, the biomarkers of beige adipose tissue were up-regulated in WAT in GTE-given groups. GTE induced genes involved in different pathways of browning, and reduced transducin-like enhancer protein-3 in WAT.Conclusion: Our results suggest that GTE may improve obesity through inducing browning in HED-fed rats.Abbreviations: ALT: Alanine transaminase; AST: Aspartate transaminase; BAT: Brown adipose tissue; BMP-7: Bone morphogenetic protein-7; BW: Body weight; CIDEA: Cell death activator; CPT-1: Carnitine palmitoyltransferase-1; EFP: Epididymal fat pad; FFA: Free fatty acid; FGF-21: Fibroblast growth factor-21; GTE: Green tea extract; HDL: High-density lipoprotein; HED: high-energy diet; LDL: Low-density lipoprotein; MFP: Mesenteric fat pad; PGC-1α: Activates PPAR-γ coactivator-1; PPAR-γ: Peroxisome proliferator-activated receptor-γ; PRDM-16: PR domain containing 16; RFP: Renal fat pad; SD: Sprague Dawley; TC: Total cholesterol; TG: Triacylglycerol; TLE-3: Transducin-like enhancer protein-3: UCP-1: Uncoupling protein-1; WAT: White adipose tissue.
Highlights
Obesity is one of the major risk factors for pathological disorders, including diabetes, hypertension, atherosclerosis, and cancer [1,2]
green tea extract (GTE) treatment resulted in significant decreases in TG, total cholesterol (TC), low-density lipoprotein (LDL), free fatty acid (FFA), aspartate transaminase (AST), alanine transaminase (ALT), and FFA, and an increase of highdensity lipoprotein (HDL) in both the 1X and 2X groups compared to the HE group
We provide evidence that GTE significantly improved obesity phenomena, such as body weight (BW), fat weight, the adipocyte size, and plasma chemical parameters in rats with high-energy diet (HED)-induced obesity
Summary
Obesity is one of the major risk factors for pathological disorders, including diabetes, hypertension, atherosclerosis, and cancer [1,2]. Green tea and its extracts were suggested to reduce body weight (BW) through inducing apoptosis, inhibiting adipogenesis, preventing energy uptake, enhancing lipolysis, elevating fatty acid oxidation-related genes, and increasing energy expenditure [7,8]. The effect of green tea on the browning of white adipose tissues (WAT) of Sprague Dawley (SD) rats is still unreported. Browning of white adipose tissue (WAT) has been reported to attenuate obesity, no study has disclosed the effects of GTE on browning in Sprague Dawley rats. Results: GTE modulated HED-induced body weight, fat accumulation, and serum levels of triacylglycerol, total cholesterol, low-density lipoprotein, free fatty acids, aspartate aminotransferase, and alanine aminotransferase. GTE induced genes involved in different pathways of browning, and reduced transducinlike enhancer protein-3 in WAT. Conclusion: Our results suggest that GTE may improve obesity through inducing browning in HED-fed rats
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