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Position: Home > Articles > Advances in Molecular Mechanisms of Tea Polyphenols in Preventing Type 2 Diabetes Mellitus Journal of Tea Science 2015 (3) 239-247

茶多酚防治2型糖尿病的分子机理研究进展

作  者：
高媛圆;毛立民;徐平;王岳飞
单  位：
浙江省茶叶学会;浙江大学茶学系
关键词：
茶多酚;EGCG;2型糖尿病;分子机理
摘  要：
茶多酚作为天然功能性物质能有效防治2型糖尿病,但是其具体作用机制仍不太清楚。研究表明它的作用机理主要是通过调控糖代谢平衡:包括降低α-糖苷酶、α-淀粉酶等双糖酶活性,调控胰岛素信号传导途径及AMPK途径中多个分子靶点的磷酸化水平,影响酶与转录因子的活性与表达,减弱胰岛素抵抗及糖异生作用,促进胰岛素的合成与分泌,促进靶组织对葡萄糖的吸收与利用等;同时,茶多酚能够调控脂代谢,通过抑制脂质合成与积累的相关酶的活性及转录因子的表达,促进脂质的氧化代谢,减轻脂代谢紊乱;另外,茶多酚的抗氧化与抗炎作用可以有效减轻组织细胞的氧化伤害和炎症损伤,减少细胞凋亡。
译  名：
Advances in Molecular Mechanisms of Tea Polyphenols in Preventing Type 2 Diabetes Mellitus
作  者：
GAO Yuanyuan;MAO Limin;XU Ping;WANG Yuefei;Department of Tea Science,Zhejiang Univerisity;Zhejiang Tea Science Society;
关键词：
tea polyphenols,EGCG,type 2 diabetes mellitus,molecular mechanism
摘  要：
As natural functional materials, tea polyphenols have been shown to effectively prevent the development of type 2 diabetes mellitus(T2DM), but the mechanism of action is still unclear. For further study, this article summarizes the molecular mechanisms implicated in th e beneficial metabolic effects of tea polyphenols. In the respect of glycometabolism, tea polyphenols significantly reduce the absorption of simple sugars by inhibiting disaccharidases(α-amylase and α-glucosidase). Then, tea polyphenols can ameliorate insulin resistance and inhibit gluconeogenesis via insulin signaling and AMPK pathway, including regulation of the phosphorylation and expression of protein kinases, and relevant transcription factors. In addition, tea polyphenols stimulate glucose uptake and utilization by increasing insulin secretion. Meanwhile, tea polyphenols showed great effects on improving lipid metabolic disorder by suppressing lipid synthesis and accumulating the activity of related enzyme and the expression of transcription factors as well as stimulating the oxidative metabolism of fat and lipid and suppressing the lipidosis. Moreover, tea polyphenols showed antioxidative and anti-inflammatory capability to ameliorate cell damage and apoptosis induced by oxidation and inflammation.

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