Skip to main content
. Author manuscript; available in PMC: 2018 Feb 1.
Published in final edited form as: Nat Rev Endocrinol. 2017 May 19;13(8):445–457. doi: 10.1038/nrendo.2017.42

Figure 6. Early-life exposure to EDCs trigger the development of NAFLD.

Figure 6

Exposure to endocrine-disrupting chemicals (EDCs) during the prenatal period (a critical ‘window of susceptibility’) can result in changes to the liver epigenome that influence susceptibility to liver disease in adulthood. The activity of epigenetic ‘writers’ of DNA (DNA methyltransferases; DNMTs) or histone (histone methyltransferases; HMTs) methyl marks (Me) or ‘erasers’ of these heritable marks (ten-eleven translocation (TET) or histone demethylases (HDMs), respectively) can be influenced by a prenatal EDC exposure, which changes their activity and alters the epigenome. Such epigenetic reprogramming could confer a propensity to develop nonalcoholic fatty liver disease (NAFLD) in adulthood via reprogrammed expression of genes involved in lipid homeostasis.