Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice.
<h4>Rationale</h4>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.<h4>Objectives</h4>We hypothesized that prenatal PAH over-expo...
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oai:doaj.org-article:13b70389bb944b83b6e551fccd3382882021-11-25T05:55:15ZPrenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice.1932-620310.1371/journal.pone.0110706https://doaj.org/article/13b70389bb944b83b6e551fccd3382882014-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0110706https://doaj.org/toc/1932-6203<h4>Rationale</h4>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.<h4>Objectives</h4>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.<h4>Materials and methods</h4>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.<h4>Findings</h4>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.<h4>Conclusions</h4>Greater prenatal PAH exposure was associated with increased weight, fat mass, adipose gene expression and epigenetic changes in progeny.Zhonghai YanHanjie ZhangChristina MaherEmilio Arteaga-SolisFrances A ChampagneLicheng WuJacob D McDonaldBeizhan YanGary J SchwartzRachel L MillerPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 10, p e110706 (2014) |
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Medicine R Science Q Zhonghai Yan Hanjie Zhang Christina Maher Emilio Arteaga-Solis Frances A Champagne Licheng Wu Jacob D McDonald Beizhan Yan Gary J Schwartz Rachel L Miller Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice. |
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<h4>Rationale</h4>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.<h4>Objectives</h4>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.<h4>Materials and methods</h4>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.<h4>Findings</h4>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.<h4>Conclusions</h4>Greater prenatal PAH exposure was associated with increased weight, fat mass, adipose gene expression and epigenetic changes in progeny. |
format |
article |
author |
Zhonghai Yan Hanjie Zhang Christina Maher Emilio Arteaga-Solis Frances A Champagne Licheng Wu Jacob D McDonald Beizhan Yan Gary J Schwartz Rachel L Miller |
author_facet |
Zhonghai Yan Hanjie Zhang Christina Maher Emilio Arteaga-Solis Frances A Champagne Licheng Wu Jacob D McDonald Beizhan Yan Gary J Schwartz Rachel L Miller |
author_sort |
Zhonghai Yan |
title |
Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice. |
title_short |
Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice. |
title_full |
Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice. |
title_fullStr |
Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice. |
title_full_unstemmed |
Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice. |
title_sort |
prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (ppar) γ methylation in offspring, grand-offspring mice. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2014 |
url |
https://doaj.org/article/13b70389bb944b83b6e551fccd338288 |
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