（-）-Epigallocatechin-3-gallate（EGCG）通过直接或间接激活糖尿病小鼠的PXR / CAR介导的II期代谢来抑制淀粉消化并改善葡萄糖稳态<a href="#fn1" title="提供电子补充信息（ESI）。参见DOI：10.1039 / c8fo01293h">†</a>,Food & Function

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（-）-Epigallocatechin-3-gallate（EGCG）通过直接或间接激活糖尿病小鼠的PXR / CAR介导的II期代谢来抑制淀粉消化并改善葡萄糖稳态 †
Food & Function ( IF 5.1 ) Pub Date : 2018-08-14 00:00:00 , DOI: 10.1039/c8fo01293h
Xiaopeng Li _{1,

2,

3,

4} , Shuyi Li _{3,

4,

5,

6} , Mo Chen _{2,

3,

4,

7} , Jingyi Wang _{1,

2,

3,

4} , Bijun Xie _{1,

2,

3,

4} , Zhida Sun _{1,

2,

3,

4}

Affiliation

（-）-epigallocatechin-3-gallate（EGCG）作为绿茶的主要成分，由于它有潜力抵抗各种人类疾病，包括肥胖症和糖尿病患者中异常的葡萄糖代谢，因此引起了科学家的关注。本研究旨在（1）评估EGCG在EGCG吸收前淀粉消化中的分子机制；（2）研究EGCG转运至小肠和肝脏后PXR / CAR介导的II期代谢与葡萄糖稳态之间的关系。EGCG抑制淀粉水解既在体外和体内。分子模拟结果表明，EGCG可以与α-淀粉酶和α-葡萄糖苷酶的活性位点结合，起抑制剂的作用。此外，在高脂饮食和STZ诱导的2型糖尿病中研究了EGCG的抗糖尿病作用。EGCG改善了葡萄糖的体内稳态，并抑制了肝脏中糖异生（PEPCK和G-6-Pase）和脂肪生成（SREBP-1C，FAS和ACC1）的过程。同时，EGCG治疗激活了PXR / CAR，并伴随着PXR / CAR介导的小肠和肝脏中II期药物代谢酶表达的提高，涉及SULT1A1，UGT1A1和SULT2B1b。饮食中的多酚EGCG可以作为有前途的PXR / CAR激活剂和糖尿病的治疗干预手段。

"点击查看英文标题和摘要"

(−)-Epigallocatechin-3-gallate (EGCG) inhibits starch digestion and improves glucose homeostasis through direct or indirect activation of PXR/CAR-mediated phase II metabolism in diabetic mice†

As a major component of green tea, (−)-epigallocatechin-3-gallate (EGCG) has attracted interest from scientists owing to its potential to combat a variety of human diseases including abnormal glucose metabolism in obesity and diabetes. This study aims to (1) evaluate the molecular mechanism of EGCG in starch digestion before EGCG absorption; (2) investigate the link between PXR/CAR-mediated phase II metabolism and glucose homeostasis after EGCG is transported to small intestine and liver. EGCG suppressed starch hydrolysis both in vitro and in vivo. Molecular simulation results demonstrated that EGCG could bind to the active site of α-amylase and α-glucosidase, acting as an inhibitor. In addition, the anti-diabetic action of EGCG was investigated in high fat diet and STZ-induced type 2 diabetes. EGCG improved glucose homeostasis and inhibited the process of gluconeogenesis (PEPCK and G-6-Pase) and lipogenesis (SREBP-1C, FAS and ACC1) in the liver. Meanwhile, EGCG treatment activated PXR/CAR, accompanied by upgrading PXR/CAR-mediated phase II drug metabolism enzyme expression in small intestine and liver, involving SULT1A1, UGT1A1 and SULT2B1b. Dietary polyphenol EGCG could serve as a promising PXR/CAR activator and therapeutic intervention in diabetes.

更新日期：2018-08-14

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