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Title: Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice.

Authors: Yan, Zhonghai; Zhang, Hanjie; Maher, Christina; Arteaga-Solis, Emilio; Champagne, Frances A; Wu, Licheng; McDonald, Jacob D; Yan, Beizhan; Schwartz, Gary J; Miller, Rachel L

Published In PLoS One, (2014)

Abstract: Greater levels of prenatal exposure to polycyclic aromatic hydrocarbon (PAH) have been associated with childhood obesity in epidemiological studies. However, the underlying mechanisms are unclear.We hypothesized that prenatal PAH over-exposure during gestation would lead to weight gain and increased fat mass in offspring and grand-offspring mice. Further, we hypothesized that altered adipose gene expression and DNA methylation in genes important to adipocyte differentiation would be affected.Pregnant dams were exposed to a nebulized PAH mixture versus negative control aerosol 5 days a week, for 3 weeks. Body weight was recorded from postnatal day (PND) 21 through PND60. Body composition, adipose cell size, gene expression of peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding proteins (C/EBP) α, cyclooxygenase (Cox)-2, fatty acid synthase (FAS) and adiponectin, and DNA methylation of PPAR γ, were assayed in both the offspring and grand-offspring adipose tissue.Offspring of dams exposed to greater PAH during gestation had increased weight, fat mass, as well as higher gene expression of PPAR γ, C/EBP α, Cox2, FAS and adiponectin and lower DNA methylation of PPAR γ. Similar differences in phenotype and DNA methylation extended through the grand-offspring mice.Greater prenatal PAH exposure was associated with increased weight, fat mass, adipose gene expression and epigenetic changes in progeny.

PubMed ID: 25347678 Exiting the NIEHS site

MeSH Terms: Adipocytes/cytology; Adiponectin/genetics; Adiponectin/metabolism; Adiposity/drug effects*; Adiposity/genetics*; Animals; Body Weight/genetics; CCAAT-Enhancer-Binding Proteins/genetics; CCAAT-Enhancer-Binding Proteins/metabolism; Cell Size; CpG Islands; Cyclooxygenase 2/genetics; Cyclooxygenase 2/metabolism; DNA Methylation*; Disease Models, Animal; Female; Gene Expression; Maternal Exposure*; Mice; PPAR gamma/genetics*; PPAR gamma/metabolism; Pediatric Obesity/etiology; Pediatric Obesity/metabolism; Phenotype; Polycyclic Aromatic Hydrocarbons/adverse effects*; Pregnancy; Prenatal Exposure Delayed Effects*; fas Receptor/genetics; fas Receptor/metabolism

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