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Background  The potential health effects of polybrominated diphenyl ethers (PBDEs) that are widely used as flame-retardants in consumer products have been attributed, in part, to their endocrine disrupting properties. The purpose of this study is to examine the  in vivo  effects of an early exposure to PBDEs on the development of insulin resistance in mice.    Results  The metabolic consequences of BDE-47 in mice with varying insulin sensitivities secondary to liver-specific activation of Akt ( Pten  fl/fl ; Alb  Cre ) and mTORC1 ( Tsc1  fl/fl ; Alb  Cre ) as well as wild-type littermates, were studied. BDE-47, a dominant congener of PBDE, was given daily (1 mg/kg/day) for six weeks by oral gavage in young mice following weaning.  At the end of the exposure, there were no significant differences in total body, liver, or white adipose tissue weights between the BDE-47-treated vs. DMSO-treated mice for each respective genotype. Metabolic studies revealed significant impairment in insulin sensitivity in the BDE-47-treated  Pten  fl/fl ; Alb  Cre  mice, but not in wild-type or  Tsc1  fl/fl ; Alb  Cre  mice. This was not accompanied by significant alterations in plasma insulin levels or hepatic triglyceride accumulation in the  Pten  fl/fl ; Alb  Cre  mice. The mean plasma BDE-47 level in the wild-type mice was 11.7 ± 2.9 ng/g (wet weight).    Conclusions  Our findings indicate that BDE-47 exposure during the early post-natal period induces a mild disturbance in glucose metabolism in susceptible mice with increased baseline insulin sensitivity. These results suggest an interaction between BDE-47 and genetic factors that regulate insulin signaling, which may result in long-term consequences.

Polybrominated diphenyl ether congener, BDE-47, impairs insulin sensitivity in mice with liver-specific Pten deficiency