Published online Aug 15, 2021. doi: 10.4239/wjd.v12.i8.1267
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
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.
The research of BDE-209 on the body's adipocyte factor and insulin sensitivity is still not fully developed.
To investigate the effects of BDE-209 on IR and glucose and lipid metabolism in C57BL/6 mice.
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.
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.
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.
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.