Basic Study
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Aug 15, 2021; 12(8): 1267-1281
Published online Aug 15, 2021. doi: 10.4239/wjd.v12.i8.1267
Decabromodiphenyl ether causes insulin resistance and glucose and lipid metabolism disorders in mice
Ayiguli Alimu, Haiqiemuhan Abudureman, Yong-Zhi Wang, Mei-Yan Li, Jia-Sui Wang, Zao-Ling Liu
Ayiguli Alimu, Haiqiemuhan Abudureman, Mei-Yan Li, Jia-Sui Wang, Zao-Ling Liu, Department of Epidemiology and Health Statistics, School of Public Health, Xinjiang Medical University, Urumqi 0991, Xinjiang Uygur Autonomous Region, China
Yong-Zhi Wang, Department of Public Health, Xinjiang Second Medical College, Cremayi 834000, Xinjiang Uygur Autonomous Region, China
Author contributions: Liu ZL participated in research design; Alimu A, Abudureman H, Wang ZW, Li MY, and Wang JS conducted the experiments; Alimu A and Liu ZL performed data analysis; Alimu A and Liu ZL wrote or edited the manuscript.
Supported by National Natural Science Foundation of China, No. 81760596; and Natural Science Foundation of Xinjiang Uygur Autonomous Region, No. 2019D01C209.
Institutional review board statement: Our research protocol was evaluated and approved by the Ethics Review Committee of the First Affiliated Hospital of Xinjiang Medical University (No. 20170214-107).
Institutional animal care and use committee statement: The animals were handled in accordance with the Guide for the Care and Use of Laboratory Animals.
Conflict-of-interest statement: No conflict of interest exits in the submission of this manuscript, and the manuscript has been approved by all authors for publication.
Data sharing statement: No other data available.
ARRIVE guidelines statement: I has read the "ARRIVE Guidelines" and has compiled and revised the manuscript according to the "ARRIVE Guidelines".
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Zao-Ling Liu, PhD, Professor, Department of Epidemiology and Health Statistics, School of Public Health, Xinjiang Medical University, No. 393 Xinyi Road, Xinshi District, Urumqi 0991, Xinjiang Uygur Autonomous Region, China. 136497460@qq.com
Received: December 18, 2020
Peer-review started: December 18, 2020
First decision: May 3, 2021
Revised: May 15, 2021
Accepted: June 25, 2021
Article in press: June 25, 2021
Published online: August 15, 2021
Processing time: 233 Days and 5.2 Hours
ARTICLE HIGHLIGHTS
Research background

Decabromodiphenyl ether (BDE-209) is the most commonly used brominated flame retardant. Recently, BDE-209 has been suspected of being an environmental risk factor for metabolic diseases such as obesity, insulin resistance (IR), type 2 diabetes mellitus, and hypertension. Data suggest that it may play a key role in the occurrence, development, and treatment of these diseases. The underlying mechanism may be that BDE-209 inappropriately regulates the number and volume of adipocytes at the molecular level, leading to adipogenesis and lipid metabolism disorders. These changes further alter the function of metabolic disease-related factors, leading to disease occurrence.

Research motivation

The research of BDE-209 on the body's adipocyte factor and insulin sensitivity is still not fully developed.

Research objectives

To investigate the effects of BDE-209 on IR and glucose and lipid metabolism in C57BL/6 mice.

Research methods

Adult male C57BL/6 mice were randomly divided into high, medium-high, medium, medium-low, and low dose BDE-209 groups, as well as a control group. After BDE-209 exposure for 60 d, the mice were fasted overnight, and then sacrificed to obtain tissues and serum to detect serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high density lipoprotein cholesterol (HDL-C) contents, and fasting insulin (FINS), leptin (LEP), and adiponectin (Adp) levels. Morphological changes of the liver were observed by hematoxylin and eosin staining. Real-time quantitative polymerase chain reaction and Western blot were used to determine the mRNA and protein levels of LEP, Adp, and peroxisome proliferators activated receptor-γ (PPARγ) in mouse liver and adipose tissues.

Research results

There was a statistically significant difference in the weight of mice in each group after 45 and 60 d of exposure. After 60 d of exposure, the weight of liver and adipose tissues in the exposure groups were greater than that in the control group. The liver tissue structure was disordered, and the liver tissues of the high, medium-high, and medium dose groups were accompanied by local inflammatory cell infiltration. Serum levels of FINS, insulin sensitivity index, Adp, and HDL-C were decreased in the BDE-209 groups compared with the control group, as were the mRNA and protein levels of Adp in liver and adipose tissues. Serum level of fasting blood glucose and LEP were higher in the BDE-209 group than in controls. TC, TG, and LDL-C levels and the mRNA and protein expression of LEP and PPARγ in liver and adipose tissue were higher than those in the control group. Homeostatic assessment model of FINS resistance was higher in the BDE-209 medium and medium-low dose groups.

Research conclusions

BDE-209 increases mouse body weight, body fat, liver tissue weight, TC, TG, and LDL-C. BDE-209 also reduces HDL-C and cause IR in mice, which may be related to activating the PPARγ receptor.

Research perspectives

Further studies on mouse serum biochemical indicators, FINS content, and adipocytokines are needed to better explore the relationship between BDE-209 and insulin sensitivity and adipocytokines.