Chen Li-Han, Chien Yi-Wen, Liang Chung-Tiang, Chan Ching-Hung, Fan Meng-Han, Huang Hui-Yu
YongLin Biomedical Engineering Center, National Taiwan University, Taipei City, Taiwan.
School of Nutrition and Health Sciences, Taipei Medical University, Taipei City, Taiwan.
Food Nutr Res. 2017 Jul 14;61(1):1347480. doi: 10.1080/16546628.2017.1347480. eCollection 2017.
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. The aims of the study were to investigate the effects of GTE on anti-obesity and browning, and their underlying mechanisms. 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. 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. Our results suggest that GTE may improve obesity through inducing browning in HED-fed rats. : 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.
大量研究报道了绿茶提取物（GTE）的抗肥胖作用。虽然已有报道称白色脂肪组织（WAT）褐变可减轻肥胖，但尚无研究揭示GTE对Sprague Dawley大鼠WAT褐变的影响。本研究的目的是探讨GTE对肥胖及褐变的影响及其潜在机制。使用了四组大鼠（每组n = 10），包括给予赋形剂的正常饮食组，以及给予赋形剂或GTE的高能饮食（HED）组，GTE通过口服灌胃给予，剂量为77.5或155 mg/kg/天，持续8周。通过体重、脂肪堆积和血清生化参数来评估肥胖情况。使用RT-qPCR和蛋白质免疫印迹法分析基因表达。GTE调节了HED诱导的体重、脂肪堆积以及血清三酰甘油、总胆固醇、低密度脂蛋白、游离脂肪酸、天冬氨酸转氨酶和丙氨酸转氨酶水平。此外，GTE提高了血清高密度脂蛋白水平。最重要的是，给予GTE组的WAT中米色脂肪组织的生物标志物上调。GTE诱导了参与不同褐变途径的基因表达，并降低了WAT中转导素样增强子蛋白-3（TLE-3）的表达。我们的结果表明，GTE可能通过诱导HED喂养大鼠的WAT褐变来改善肥胖。：ALT：丙氨酸转氨酶；AST：天冬氨酸转氨酶；BAT：棕色脂肪组织；BMP-7：骨形态发生蛋白-7；BW：体重；CIDEA：细胞死亡激活剂；CPT-1：肉碱棕榈酰转移酶-1；EFP：附睾脂肪垫；FFA：游离脂肪酸；FGF-21：成纤维细胞生长因子-21；GTE：绿茶提取物；HDL：高密度脂蛋白；HED：高能饮食；LDL：低密度脂蛋白；MFP：肠系膜脂肪垫；PGC-1α：过氧化物酶体增殖物激活受体γ共激活因子-1；PPAR-γ：过氧化物酶体增殖物激活受体γ；PRDM-16：含PR结构域的蛋白16；RFP：肾脂肪垫；SD：Sprague Dawley；TC：总胆固醇；TG：三酰甘油；TLE-3：转导素样增强子蛋白-3；UCP-1：解偶联蛋白-1；WAT：白色脂肪组织
