Decabromodiphenyl ether (decaBDE) is a brominated flame retardant used in plastic and textile articles. It has become a ubiquitous environmental contaminant, however; the relationship between decaBDE and obesity remains to be elucidated. We aimed to clarify if oral decaBDE exposure can be a factor in obesity and its related metabolic dysfuctions. Male C57BL/6 J mice were fed a normal (ND, 9.0 kcal% fat) or high-fat (HFD, 62.2 kcal% fat) diet and treated with decaBDE (the equivalent of three doses of 0, 0.5 (L-DecaBDE), and 10 (H-DecaBDE) μg/kg body weight/day) ad libitum in drinking water from 5 to 20 weeks of age. In HFD-fed mice, decaBDE exposure markedly increased both fasting blood glucose levels compared with vehicle exposure, which was more prominent in H-DecaBDE-exposed mice. DecaBDE exposure significantly reduced mRNA levels of glucose transporter 4 and thyroid hormone receptor alpha in skeletal muscle and mechanistic target of rapamycin complex 2 in brown adipose tissue compared with vehicle exposure under HFD-feeding. The tendency for hyperglycemia and the remarkable activation of insulin signaling pathway-related genes were observed in ND + DecaBDE mice compared to the ND + Vehicle mice. These results demonstrate that decaBDE can contribute to the enhancement of diet-induced hyperglycemia through disruption of glucose homeostasis.
Keywords: Brominated flame retardant; Decabromodiphenyl ether; Glucose homeostasis; Hyperglycemia; Obesity.
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