Studies have shown that perinatal exposure of rats and mice to common flame retardants found in household items permanently reprograms liver metabolism, often leading later in life to insulin resistance and non-alcoholic fatty liver disease.

Now, research led by University of Massachusetts Amherst environmental toxicologist Alexander Suvorov, with co-authors in Moscow, Russia, has identified the likely mechanism responsible for the pollutant’s effect: an altered liver epigenome. The epigenome refers to heritable changes in gene expression without changes in the DNA sequence. “Changes in the liver epigenome can explain those functional changes in the liver,” Suvorov explains. “We looked at two different epigenetic mechanisms and there were changes in both.”

Published Dec. 13 in the medical journal Epigenomics, the study showed that environmentally relevant exposure to polybrominated diphenyl ether (PBDE) through the umbilical cord and breast milk permanently changed liver metabolism in rats. The mother rats were fed enough PBDEs to cause concentrations in their fat similar to those found in humans living in big cities in the U.S.



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