Format

Send to

Choose Destination
J Gastroenterol. 2016 Aug;51(8):819-29. doi: 10.1007/s00535-015-1154-0. Epub 2016 Jan 21.

Pu-erh tea extract ameliorates high-fat diet-induced nonalcoholic steatohepatitis and insulin resistance by modulating hepatic IL-6/STAT3 signaling in mice.

Author information

1
Division of Hepatobiliary and Pancreatic Diseases, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
2
Department of Pu-erh Tea and Medical Science, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
3
Department of Microbiology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
4
Key Laboratory of Pu-erh Tea Science, The Ministry of Education, Yunnan Agricultural University, Kunming, 650201, People's Republic of China.
5
Yunnan University, Kunming, 650091, People's Republic of China.
6
Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, 606-8502, Japan.
7
Division of Hepatobiliary and Pancreatic Diseases, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan. nishiguc@hyo-med.ac.jp.
8
Key Laboratory of Pu-erh Tea Science, The Ministry of Education, Yunnan Agricultural University, Kunming, 650201, People's Republic of China. shengjunpuer@yahoo.com.cn.

Abstract

BACKGROUND:

Pu-erh tea, made from the leaves of Camellia sinensis, possesses activities beneficial for human health, including anti-inflammatory, anti-oxidant, and anti-obesity properties.

OBJECTIVE:

We investigated the effects of a pu-erh tea extract (PTE) on nonalcoholic steatohepatitis (NASH) and the molecular mechanisms underlying such effects.

METHODS:

Eight-week-old male C57BL/6J mice were fed a normal chow diet or high-fat diet (HFD) for 17 weeks, during which PTE was simultaneously administered in drinking water. Body weight, hepatic inflammation, steatosis, insulin sensitivity, expression of lipogenesis- and gluconeogenesis-associated genes, and signal transducer and activator of transcription (STAT)-3 phosphorylation were examined. The anti-steatotic effects of PTE and/or interleukin (IL)-6 were evaluated in HepG2 cells. The lipid accumulation, STAT3 phosphorylation, and expression of lipid metabolism-related genes were analyzed.

RESULTS:

PTE inhibited HFD-induced obesity and significantly attenuated HFD-induced hepatic steatosis and liver inflammation, and prevented against liver injury. PTE treatment improved glucose tolerance and insulin sensitivity in HFD-fed mice. Moreover, PTE treatment maintained the intact insulin signal and significantly decreased expression of gluconeogenesis-related genes in the livers of HFD-fed mice. PTE treatment strikingly enhanced STAT3 phosphorylation in the livers of HFD-fed mice. Consistent with this increase in STAT3 phosphorylation, pre-treatment of HepG2 cells with PTE enhanced IL-6-induced STAT3 phosphorylation and attenuated oleic acid-induced steatosis in a STAT3-dependent manner. In contrast, PTE inhibited IL-6-induced STAT3 phosphorylation in macrophages.

CONCLUSIONS:

PTE ameliorates hepatic lipid metabolism, inflammation, and insulin resistance in mice with HFD-induced NASH, presumably by modulating hepatic IL-6/STAT3 signaling.

KEYWORDS:

Insulin resistance; NASH; PTE; STAT3

PMID:
26794005
DOI:
10.1007/s00535-015-1154-0
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center