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绿茶表没食子儿茶素没食子酸酯对内分泌系统和食物摄入的调节作用。

Modulation of endocrine systems and food intake by green tea epigallocatechin gallate.

作者信息

Kao Y H, Hiipakka R A, Liao S

机构信息

Ben May Institute for Cancer Research, Department of Biochemistry and Molecular Biology, and Tang Center for Herbal Medicine Research, University of Chicago, Illinois 60637, USA.

出版信息

Endocrinology. 2000 Mar;141(3):980-7. doi: 10.1210/endo.141.3.7368.

DOI:10.1210/endo.141.3.7368
PMID:10698173
Abstract

Green tea polyphenols, especially the catechin, (-)-epigallocatechin gallate (EGCG), have been proposed as a cancer chemopreventative based on a variety of laboratory studies. For clear assessment of the possible physiological effects of green tea consumption, we injected pure green tea catechins ip into rats and studied their acute effects on endocrine systems. We found that EGCG, but not related catechins, significantly reduced food intake; body weight; blood levels of testosterone, estradiol, leptin, insulin, insulin-like growth factor I, LH, glucose, cholesterol, and triglyceride; as well as growth of the prostate, uterus, and ovary. Similar effects were observed in lean and obese male Zucker rats, suggesting that the effect of EGCG was independent of an intact leptin receptor. EGCG may interact specifically with a component of a leptin-independent appetite control pathway. Endocrine changes induced by parenteral administration of EGCG may relate to the observed growth inhibition and regression of human prostate and breast tumors in athymic mice treated with EGCG as well as play a role in the mechanism by which EGCG inhibits cancer initiation and promotion in various animal models of cancer.

摘要

基于各种实验室研究,绿茶多酚,尤其是儿茶素(-)-表没食子儿茶素没食子酸酯(EGCG),已被提议作为一种癌症化学预防剂。为了明确评估饮用绿茶可能产生的生理影响,我们将纯绿茶儿茶素腹腔注射到大鼠体内,并研究了它们对内分泌系统的急性影响。我们发现,EGCG而非相关儿茶素能显著降低食物摄入量、体重、睾酮、雌二醇、瘦素、胰岛素、胰岛素样生长因子I、促黄体生成素、葡萄糖、胆固醇和甘油三酯的血液水平,以及前列腺、子宫和卵巢的生长。在瘦型和肥胖型雄性Zucker大鼠中也观察到了类似的效果,这表明EGCG的作用独立于完整的瘦素受体。EGCG可能与不依赖瘦素的食欲控制途径的一个成分发生特异性相互作用。经肠外给予EGCG所诱导的内分泌变化,可能与在接受EGCG治疗的无胸腺小鼠中观察到的人类前列腺和乳腺肿瘤的生长抑制及消退有关,并且在EGCG抑制各种癌症动物模型中癌症起始和促进的机制中发挥作用。

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