n/a
Article Publish Status: FREE
Abstract Title:

Suppresses Body Weight Gain and Alters Expression of theGene in High-Fat-Diet Induced Obese Mice.

Abstract Source:

Biomed Res Int. 2017 ;2017:6280972. Epub 2017 Sep 20. PMID: 29098158

Abstract Author(s):

Tao Zhong, Xiao-Yue Duan, Hao Zhang, Li Li, Hong-Ping Zhang, Lili Niu

Article Affiliation:

Tao Zhong

Abstract:

The root of(RAS) is a traditional Chinese medicine used for preventing and treating various diseases. In this study, we assessed RAS supplementation effects on body weight and thegene expression and methylation status in a high-fat-diet (HFD) induced obese mouse model. Female obese mice were divided into groups according to RAS dosage in diet as follows: normal diet, HFD diet (HC), HFD with low-dosage RAS (DL), HFD with medium-dosage RAS (DM), and HFD with high-dosage RAS (DH). After RAS supplementation for 4 weeks, body weight suppression andexpression in DH mice were significantly higher than in HC mice, whereas no significant change inexpression was detected between DM and DL mice or in their offspring. Bisulfite sequencing PCR (BSP) revealed that the CpG island in thepromoter was hypermethylated up to 95.44% in the HC group, 91.67% in the DH group, and 90.00% in the normal diet group. Histological examination showed that adipocytes in the DH group were smaller than those in the HC group, indicating a potential role of RAS in obesity. This study indicated that RAS could ameliorate obesity induced by HFD and that the molecular mechanism might be associated with the expression of thegene.

Study Type : Animal Study

Print Options


Key Research Topics

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2024 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.