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J Gastroenterol. 2017 Dec;52(12):1240-1251. doi: 10.1007/s00535-017-1332-3. Epub 2017 Mar 31.

Pu'erh tea extract-mediated protection against hepatosteatosis and insulin resistance in mice with diet-induced obesity is associated with the induction of de novo lipogenesis in visceral adipose tissue.

Author information

1
Department of Internal Medicine, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
2
Department of Microbiology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.
3
Department of Pu-erh Tea and Medical Science, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.
4
Key Laboratory of Pu-erh Tea Science, The Ministry of Education, Yunnan Agricultural University, Kunming, 650201, China.
5
Yunnan University, Kunming, China.
6
State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Kunming, China.
7
Department of Internal Medicine, 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, China. shengjunpuer@yahoo.com.cn.
9
State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Kunming, China. shengjunpuer@yahoo.com.cn.
10
Pu'erh Tea Research Institute, Pu'erh, China. shengjunpuer@yahoo.com.cn.

Abstract

BACKGROUND:

White adipose tissue (WAT) is important for the maintenance of metabolic homeostasis, and metabolic syndrome is sometimes associated with WAT dysfunction in humans and animals. WAT reportedly plays a key, beneficial role in the maintenance of glucose and lipid homeostasis during de novo lipogenesis (DNL). Pu'erh tea extract (PTE) can inhibit harmful, ectopic DNL in the liver, thus protecting against hepatosteatosis, in mice with diet-induced obesity. We examined whether PTE could induce DNL in WAT and consequently protect against hepatosteatosis.

METHODS:

C57BL/6 male mice were fed a high-fat diet (HFD) with/without PTE for 16 weeks. Systemic insulin sensitivity was determined using HOMA-IR, insulin- and glucose-tolerance tests, and WAT adipogenesis was evaluated by histological analysis. Adipogenesis-, inflammation-, and DNL-related gene expression in visceral AT (VAT) and subcutaneous AT (SAT) was measured using quantitative reverse transcription-PCR. Regression analysis was used to investigate the association between DNL in WAT and systemic insulin resistance or hepatosteatosis.

RESULTS:

Pu'erh tea extract significantly reduced the gain of body weight and SAT, but not VAT adiposity, in mice fed the high-fat diet and induced adipogenesis in VAT. The expression of DNL-related genes, including Glut4, encoding an important insulin-regulated glucose transporter (GLUT4), were highly elevated in VAT. Moreover, PTE inhibited VAT inflammation by simultaneously downregulating inflammatory molecules and inducing expression of Gpr120 that encodes an anti-inflammatory and pro-adipogenesis receptor (GPR-120) that recognizes unsaturated long-chain fatty acids, including DNL products. The expression of DNL-related genes in VAT was inversely correlated with hepatosteatosis and systemic insulin resistance.

CONCLUSIONS:

Activation of DNL in VAT may explain PTE-mediated alleviation of hepatosteatosis symptoms and systemic insulin resistance.

KEYWORDS:

De novo lipogenesis; Hepatosteatosis; Insulin resistance; Pu’erh tea extract; Visceral adipose tissue

PMID:
28364190
DOI:
10.1007/s00535-017-1332-3
[Indexed for MEDLINE]

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