Theabrownin from Pu-erh tea attenuates hypercholesterolemia via modulation of gut microbiota and bile acid metabolism

Fengjie Huang, Xiaojiao Zheng, Xiaohui Ma, Runqiu Jiang, Wangyi Zhou, Shuiping Zhou, Yunjing Zhang, Sha Lei, Shouli Wang, Junliang Kuang, Xiaolong Han, Meilin Wei, Yijun You, Mengci Li, Yitao Li, Dandan Liang, Jiajian Liu, Tianlu Chen, Chao Yan, Runmin WeiCynthia Rajani, Chengxing Shen, Guoxiang Xie, Zhaoxiang Bian, Houkai Li*, Aihua Zhao*, Wei Jia*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

481 Citations (Scopus)


Pu-erh tea displays cholesterol-lowering properties, but the underlying mechanism has not been elucidated. Theabrownin is one of the most active and abundant pigments in Pu-erh tea. Here, we show that theabrownin alters the gut microbiota in mice and humans, predominantly suppressing microbes associated with bile-salt hydrolase (BSH) activity. Theabrownin increases the levels of ileal conjugated bile acids (BAs) which, in turn, inhibit the intestinal FXR-FGF15 signaling pathway, resulting in increased hepatic production and fecal excretion of BAs, reduced hepatic cholesterol, and decreased lipogenesis. The inhibition of intestinal FXR-FGF15 signaling is accompanied by increased gene expression of enzymes in the alternative BA synthetic pathway, production of hepatic chenodeoxycholic acid, activation of hepatic FXR, and hepatic lipolysis. Our results shed light into the mechanisms behind the cholesterol- and lipid-lowering effects of Pu-erh tea, and suggest that decreased intestinal BSH microbes and/or decreased FXR-FGF15 signaling may be potential anti-hypercholesterolemia and anti-hyperlipidemia therapies.

Original languageEnglish
Article number4971
JournalNature Communications
Issue number1
Publication statusPublished - Dec 2019

Scopus Subject Areas

  • Chemistry(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Physics and Astronomy(all)


Dive into the research topics of 'Theabrownin from Pu-erh tea attenuates hypercholesterolemia via modulation of gut microbiota and bile acid metabolism'. Together they form a unique fingerprint.

Cite this