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Polybrominated diphenyl ether congener, BDE-47, impairs insulin sensitivity in mice with liver-specific Pten
Rebecca L McIntyre1, Heidi L Kenerson1, Savitha Subramanian2
1Department of Surgery, University of Washington, 1959 NE Pacific, Seattle, WA 98195 USA.
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.
Insights
Early exposure to polybrominated diphenyl ethers (PBDEs) like BDE-47 can disrupt glucose metabolism in genetically susceptible mice. This endocrine disruption highlights potential long-term health risks associated with flame retardants.
Area of Science:
- Environmental Health
- Endocrinology
- Metabolic Syndrome
Background:
- Polybrominated diphenyl ethers (PBDEs) are flame retardants with potential endocrine-disrupting properties.
- PBDEs are widely used in consumer products, leading to environmental and human exposure.
- Early life exposure to environmental contaminants is a critical window for developmental toxicity.
Purpose of the Study:
- To investigate the in vivo effects of early polybrominated diphenyl ethers (PBDEs) exposure on insulin resistance development.
- To examine the impact of BDE-47, a common PBDE congener, on metabolic parameters in mice.
- To assess the role of genetic background in mediating the effects of PBDEs on insulin sensitivity.
Main Methods:
- Young mice with varying insulin sensitivities (wild-type, Akt-activated, mTORC1-activated) were exposed to BDE-47 (1 mg/kg/day) or vehicle for six weeks.
- Metabolic studies were conducted to assess insulin sensitivity, plasma insulin levels, and hepatic triglyceride accumulation.
- Genotype-specific effects of BDE-47 on body, liver, and adipose tissue weights were analyzed.
Main Results:
- BDE-47 exposure did not significantly alter body, liver, or adipose tissue weights across genotypes.
- Significant impairment in insulin sensitivity was observed in BDE-47-treated mice with liver-specific Akt activation (Pten (fl/fl);Alb (Cre)).
- No significant alterations in insulin sensitivity were found in wild-type or mTORC1-activated (Tsc1 (fl/fl);Alb (Cre)) mice, nor were plasma insulin levels or hepatic triglycerides affected.
Conclusions:
- Early post-natal BDE-47 exposure induces mild glucose metabolism disturbances in genetically susceptible mice.
- These findings suggest a gene-environment interaction between BDE-47 and insulin signaling pathways.
- This interaction may lead to long-term metabolic consequences, emphasizing the importance of early life exposure assessments.
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