Background: Environmental polybrominated diphenyl ether (PBDE) exposure may be associated with diabetes and obesity. 2,2′,4,4′,5,5′-Hexabromodiphenyl ether (BDE-153) is one of the most abundant and widely distributed homologs of PBDEs detected in humans. This study investigated the effects of BDE-153 on the expression of adipokines and glucose and lipid metabolism. Methods: Adult male C57BL/6 mice were divided into five BDE-153 groups and one control group. After BDE-153 exposure for 4 weeks, the levels of biochemical indexes and the mRNA and protein expression levels of leptin, adiponectin, peroxisome proliferators activated receptors gamma (PPARγ), and AMPKα were measured. The histomorphological changes of liver and pancreas tissues were observed. Results: After BDE-153 exposure, the weight of mice in the medium-high-dose group at different exposure times was lower than that in the control group (p all <0.05), and the body weight decreased slightly with the increase of the dose of BDE-153. BDE-153 caused the disorder of glucose and lipid metabolism in mice, the weight of liver and pancreas increased, lipid droplets accumulated in liver cells, and the positive rate of insulin staining increased in a dose-dependent manner. BDE-153 also interfered with the expression of PPARγ, AMPKα, and adipokines. The results of restrictive cubic splines (RCS) showed that there were a nonlinear dose-response relationship between the exposure dose of BDE-153 and the expression levels of PPARγ, AMPKα, and adipokines. Conclusion: Our results suggest that BDE-153 may interfere with the expression of adipokines and the secretion of insulin by affecting the expression of PPARγ and AMPKα, which play a key role in glucose and lipid metabolism, leading to the occurrence of glucose and lipid metabolism disorder.
BDE-47 (2,2,4,4-tetrabromodiphenyl ether) is a polybrominated diphenyl ether (PBDE) congener, which has the characteristics of high biological detection rate, the highest content and strong biological toxicity, and is widely distributed in organisms. Many studies have found that BDE-47 may also be an environmental risk factor for metabolic diseases such as obesity, insulin resistance, type 2 diabetes, and hypertension. However, the way that PBDEs influence adipocyte differentiation remains unclear. The methylisobutylxanthine, dexamethasone, and insulin method was used to study the effect of BDE-47 on the differentiation of 3T3-L1 cells. The 3T3-L1 cells were exposed by different concentrations of BDE-47, and the effect of cell viability was detected at different stages. In addition, the lipid droplet aggregation of adipocytes was observed and the triglyceride (TG) levels in the cytoplasm were detected after differentiation. The relative mRNA expression levels of leptin, adiponectin, and PPARγ in cells were determined by RT-PCR, and differentially expressed genes were preliminarily screened by digital gene expression profile. Our study found that BDE-47 promoted the differentiation of 3T3-L1 cells. Restriction cubic spline analysis showed that BDE-47 bidirectionally. regulated the mRNA synthesis of TG, PPARγ, and leptin genes and the aggregation of lipid droplets. BDE-47 may induce adipocyte differentiation by activating PPARγ, resulting in the differential expression of genes related to the AMPK signaling pathway, insulin resistance, and other metabolic pathways. The highest and lowest-dose BDE-47 exposure groups had the greatest impact on adipocyte differentiation.
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