The major green tea polyphenol, (-)-epigallocatechin-3-gallate, inhibits obesity, metabolic syndrome, and fatty liver disease in high-fat-fed mice.

The major green tea polyphenol, (-)-epigallocatechin-3-gallate, inhibits obesity, metabolic syndrome, and fatty liver disease in high-fat-fed mice.
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DOI:
10.1093/jn/138.9.1677
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发表时间:
2008-09
期刊:
The Journal of nutrition
影响因子:
--
通讯作者:
Yang CS
Yang CS
中科院分区:
其他
文献类型:
--
作者:
Bose M;Lambert JD;Ju J;Reuhl KR;Shapses SA;Yang CS

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在这项研究中,我们调查了主要的绿色茶多酚,(-)-表没食子儿茶素-3-没食子酸酯(EGCG),对高脂肪诱导的肥胖症,代谢综合征的症状,和脂肪肝小鼠的影响。在喂食高脂饮食(60%能量为脂肪)的小鼠中,与未接受EGCG治疗的小鼠相比,补充饮食EGCG治疗(3.2 g/kg饮食)16周降低了体重(BW)增加、体脂百分比和内脏脂肪重量(P < 0.05)。高脂组体重下降与粪便脂质增加有关(r2 = 0.521; P < 0.05)。EGCG治疗降低了高脂喂养小鼠的胰岛素抵抗、血浆胆固醇和单核细胞趋化蛋白浓度(P < 0.05)。EGCG治疗还降低了高脂喂养小鼠的肝脏重量、肝脏甘油三酯和血浆丙氨酸氨基转移酶浓度(P < 0.05)。肝脏样本的组织学分析显示,与未接受EGCG治疗的高脂饮食喂养的小鼠相比,接受EGCG治疗的小鼠肝细胞中的脂质积累减少。在另一项实验中,接受短期EGCG治疗(3.2g/kg饮食,4周)的3月龄高脂诱导的肥胖小鼠与高脂喂养的对照小鼠相比,肠系膜脂肪重量和血糖降低(P < 0.05)。我们的研究结果表明,长期的EGCG治疗减弱了肥胖,代谢综合征相关症状和脂肪肝的发展。短期EGCG治疗似乎可以逆转肥胖小鼠中预先存在的高脂肪诱导的代谢病变。这些作用可能是通过减少脂质吸收、减少炎症和其他机制介导的。
In this study, we investigated the effects of the major green tea polyphenol, (−)-epigallocatechin-3-gallate (EGCG), on high-fat–induced obesity, symptoms of the metabolic syndrome, and fatty liver in mice. In mice fed a high-fat diet (60% energy as fat), supplementation with dietary EGCG treatment (3.2 g/kg diet) for 16 wk reduced body weight (BW) gain, percent body fat, and visceral fat weight (P < 0.05) compared with mice without EGCG treatment. The BW decrease was associated with increased fecal lipids in the high-fat–fed groups (r2 = 0.521; P < 0.05). EGCG treatment attenuated insulin resistance, plasma cholesterol, and monocyte chemoattractant protein concentrations in high-fat–fed mice (P < 0.05). EGCG treatment also decreased liver weight, liver triglycerides, and plasma alanine aminotransferase concentrations in high-fat–fed mice (P < 0.05). Histological analyses of liver samples revealed decreased lipid accumulation in hepatocytes in mice treated with EGCG compared with high-fat diet-fed mice without EGCG treatment. In another experiment, 3-mo-old high-fat–induced obese mice receiving short-term EGCG treatment (3.2 g/kg diet, 4 wk) had decreased mesenteric fat weight and blood glucose compared with high-fat–fed control mice (P < 0.05). Our results indicate that long-term EGCG treatment attenuated the development of obesity, symptoms associated with the metabolic syndrome, and fatty liver. Short-term EGCG treatment appeared to reverse preexisting high-fat–induced metabolic pathologies in obese mice. These effects may be mediated by decreased lipid absorption, decreased inflammation, and other mechanisms.
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