Exposure to adverse early-life environments (AME) increases the incidence of developing adult-onset non-alcoholic fatty liver disease (NAFLD). DNA methylation has been postulated to link AME and late-onset diseases. This study aimed to investigate whether and to what extent the hepatic DNA methylome was perturbed prior to the development of NAFLD in offspring exposed to AME in mice.
View Article and Find Full Text PDFBackground: The role of an adverse maternal environment (AME) in conjunction with a postweaning Western diet (WD) in the development of nonalcoholic fatty liver disease (NAFLD) in adult offspring has not been explored. Likewise, the molecular mechanisms associated with AME-induced NAFLD have not been studied. The fatty acid translocase or cluster of differentiation 36 (CD36) has been implicated to play a causal role in the pathogenesis of WD-induced steatosis.
View Article and Find Full Text PDFChildren exposed to early-life adversity carry a greater risk of poor health and disease into adulthood. This increased disease risk is shadowed by changes in the epigenome. Epigenetics can change gene expression to modify disease risk; unfortunately, how epigenetics are changed by the environment is unclear.
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