Literature DB >> 28736228

DBZ is a putative PPARγ agonist that prevents high fat diet-induced obesity, insulin resistance and gut dysbiosis.

Pengfei Xu1, Fan Hong1, Jialin Wang1, Jing Wang1, Xia Zhao2, Sheng Wang1, Tingting Xue1, Jingwei Xu3, Xiaohui Zheng4, Yonggong Zhai5.   

Abstract

BACKGROUND: The nuclear receptor PPARγ is an effective pharmacological target for some types of metabolic syndrome, including obesity, diabetes, nonalcoholic fatty liver disease, and cardiovascular disease. However, the current PPARγ-targeting thiazolidinedione drugs have undesirable side effects. Danshensu Bingpian Zhi (DBZ), also known as tanshinol borneol ester derived from Salvia miltiorrhiza, is a synthetic derivative of natural compounds used in traditional Chinese medicine for its anti-inflammatory activity.
METHODS: In vitro, investigations of DBZ using a luciferase reporter assay and molecular docking identified this compound as a novel promising PPARγ agonist. Ten-week-old C57BL/6J mice were fed either a normal chow diet (NCD) or a high-fat diet (HFD). The HFD-fed mice were gavaged daily with either vehicle or DBZ (50mg/kg or 100mg/kg) for 10weeks. The gut microbiota composition was assessed by analyzing the 16S rRNA gene V3+V4 regions via pyrosequencing.
RESULTS: DBZ is an efficient natural PPARγ agonist that shows lower PPARγ-responsive luciferase reporter activity than thiazolidinediones, has excellent effects on the metabolic phenotype and exhibits no unwanted adverse effects in a HFD-induced obese mouse model. DBZ protects against HFD-induced body weight gain, insulin resistance, hepatic steatosis and inflammation in mice. DBZ not only stimulates brown adipose tissue (BAT) browning and maintains intestinal barrier integrity but also reverses HFD-induced intestinal microbiota dysbiosis.
CONCLUSIONS: DBZ is a putative PPARγ agonist that prevents HFD-induced obesity-related metabolic syndrome and reverse gut dysbiosis. GENERAL SIGNIFICANCE: DBZ may be used as a beneficial probiotic agent to improve HFD-induced obesity-related metabolic syndrome in obese individuals.
Copyright © 2017 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Gut microbiota; Insulin resistance; Obesity; PPARγ

Mesh:

Substances:

Year:  2017        PMID: 28736228     DOI: 10.1016/j.bbagen.2017.07.013

Source DB:  PubMed          Journal:  Biochim Biophys Acta Gen Subj        ISSN: 0304-4165            Impact factor:   3.770


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