Department of Food Science, The Pennsylvania State University, 332 Food Science Building, University Park, PA 16802, USA.
Food Funct. 2011 Feb;2(2):111-6. doi: 10.1039/c0fo00155d. Epub 2011 Jan 4.
(-)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, has been shown to prevent the development of obesity in rodent models. Here, we examined the effect of EGCG on markers of fat oxidation in high fat-fed C57bl/6J mice. High fat-fed mice treated with 0.32% dietary EGCG for 16 weeks had reduced body weight gain and final body weight (19.2% and 9.4%, respectively) compared to high fat-fed controls. EGCG-treatment decreased fasting blood glucose, plasma insulin, and insulin resistance by 18.5%, 25.3%, and 33.9%, respectively. EGCG treatment also reduced markers of obesity-related fatty liver disease in high fat-fed mice. Gene expression analysis of skeletal muscle showed that EGCG increased mRNA levels of nuclear respiratory factor (nrf)1, medium chain acyl coA decarboxylase (mcad), uncoupling protein (ucp)3, and peroxisome proliferator responsive element (ppar)α by 1.4-1.9-fold compared to high fat-fed controls. These genes are all related to mitochondrial fatty acid oxidation. In addition, EGCG increased fecal excretion of lipids in high fat-fed mice. In summary, it appears that EGCG modulates body weight gain in high fat-fed mice both by increasing the expression of genes related fat oxidation in the skeletal muscle and by modulating fat absorption from the diet.
(-)-表没食子儿茶素没食子酸酯（EGCG）是绿茶中的主要多酚，已被证明可预防肥胖症在啮齿动物模型中的发展。在这里，我们研究了 EGCG 对高脂肪喂养 C57bl/6J 小鼠脂肪氧化标志物的影响。用 0.32％饮食 EGCG 治疗 16 周的高脂肪喂养的小鼠与高脂肪喂养的对照组相比，体重增加和最终体重分别降低了 19.2％和 9.4％。EGCG 治疗可使空腹血糖，血浆胰岛素和胰岛素抵抗分别降低 18.5％，25.3％和 33.9％。EGCG 治疗还可降低高脂肪喂养小鼠肥胖相关脂肪性肝病的标志物。骨骼肌的基因表达分析表明，与高脂肪喂养的对照组相比，EGCG 使核呼吸因子（nrf）1，中链酰基辅酶 A 脱羧酶（mcad），解偶联蛋白（ucp）3 和过氧化物酶体增殖物激活受体反应元件（ppar）α的 mRNA 水平分别增加了 1.4-1.9 倍。这些基因都与线粒体脂肪酸氧化有关。此外，EGCG 增加了高脂肪喂养小鼠粪便中脂质的排泄。总之，似乎 EGCG 通过增加骨骼肌中与脂肪氧化有关的基因的表达并调节饮食中脂肪的吸收，来调节高脂肪喂养小鼠的体重增加。
