The effects of decabromodiphenyl ether on glycolipid metabolism and related signaling pathways in mice.

Decabromodiphenyl ether (BDE-209), an addictive type flame retardant, is widely found in environments, and could affect the glycolipid metabolism. The present study was designed to investigate the potential mechanism of BDE-209 affecting glycolipid metabolism. Forty mice were randomly divided into four groups, and they were exposed to BDE-209 at dosages of 0, 7.5, 25 and 75 mg kg·d for 28 d, respectively. The results showed that BDE-209 increased the serum levels of glucose, insulin, and triglyceride, also decreased the level of high-density lipoprotein, and damaged the structures of liver and adipose tissue in mice. BDE-209 significantly increased the protein expression of p-IRS, markedly decreased the expressions of PI3K, p-AKT, and GLUT4, significantly improved the lipid metabolism related factor expressions of p-mTOR, mTOR, PPARγ and RXRɑ, also inhibited the activity of antioxidant enzymes in the liver of mice. These results suggested that BDE-209 could affect glucose metabolism and inhibiting PI3K/AKT/GLUT4 signaling pathway resulting from improving the p-IRS expression, and interfered with lipid metabolism through activate mTOR/PPARγ/RXRα resulting from oxidative stress in mice.