Lee Mak-Soon, Kim Chong-Tai, Kim Yangha
Department of Nutritional Science and Food Management, Ewha Womans University, Seoul, Korea.
Ann Nutr Metab. 2009;54(2):151-7. doi: 10.1159/000214834. Epub 2009 Apr 22.
The aim of this study was to investigate the antiobesity effect of (-)-epigallocatechin-3-gallate (EGCG) in diet-induced obese mice.
Male C57BL/6J mice were fed on a high-fat diet for 8 weeks to induce obesity. Subsequently they were divided into 3 groups and were maintained on a high-fat control diet or high-fat diets supplemented with 0.2 or 0.5% EGCG (w/w) for a further 8 weeks. Changes in the expression of genes related to lipid metabolism and fatty acid oxidation were analyzed in white adipose tissue, together with biometric and blood parameters.
Experimental diets supplemented with EGCG resulted in reduction of body weight and mass of various adipose tissues in a dose-dependent manner. EGCG diet also considerably lowered the levels of plasma triglyceride and liver lipid. In the epididymal white adipose tissue of EGCG diet-fed mice, the mRNA levels of adipogenic genes such as peroxisome proliferator-activated receptor-gamma (PPAR-gamma), CCAAT enhancer-binding protein-alpha (C/EBP-alpha), regulatory element-binding protein-1c (SREBP-1c), adipocyte fatty acid-binding protein (aP2), lipoprotein lipase (LPL) and fatty acid synthase (FAS) were significantly decreased. However, the mRNA levels of carnitine palmitoyl transferase-1 (CPT-1) and uncoupling protein 2 (UCP2), as well as lipolytic genes such as hormone sensitive lipase (HSL) and adipose triglyceride lipase (ATGL), were significantly increased.
These results suggest that green tea EGCG effectively reduces adipose tissue mass and ameliorates plasma lipid profiles in high-fat diet-induced obese mice. These effects might be at least partially mediated via regulation of the expression of multiple genes involved in adipogenesis, lipolysis, beta-oxidation and thermogenesis in white adipose tissue.
本研究旨在探讨(-)-表没食子儿茶素-3-没食子酸酯(EGCG)对饮食诱导肥胖小鼠的抗肥胖作用。
雄性C57BL/6J小鼠喂食高脂饮食8周以诱导肥胖。随后将它们分为3组,并继续喂食高脂对照饮食或补充0.2%或0.5%(w/w)EGCG的高脂饮食8周。分析白色脂肪组织中与脂质代谢和脂肪酸氧化相关基因的表达变化,以及生物特征和血液参数。
补充EGCG的实验饮食导致体重和各种脂肪组织质量呈剂量依赖性降低。EGCG饮食还显著降低了血浆甘油三酯和肝脏脂质水平。在喂食EGCG饮食的小鼠附睾白色脂肪组织中,过氧化物酶体增殖物激活受体-γ(PPAR-γ)、CCAAT增强子结合蛋白-α(C/EBP-α)、调节元件结合蛋白-1c(SREBP-1c)、脂肪细胞脂肪酸结合蛋白(aP2)、脂蛋白脂肪酶(LPL)和脂肪酸合酶(FAS)等脂肪生成基因的mRNA水平显著降低。然而,肉碱棕榈酰转移酶-1(CPT-1)和解偶联蛋白2(UCP2)的mRNA水平,以及激素敏感脂肪酶(HSL)和脂肪甘油三酯脂肪酶(ATGL)等脂解基因的mRNA水平显著升高。
这些结果表明,绿茶EGCG可有效减少高脂饮食诱导肥胖小鼠的脂肪组织质量,并改善血浆脂质谱。这些作用可能至少部分是通过调节白色脂肪组织中参与脂肪生成、脂解、β氧化和产热的多个基因的表达来介导的。