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

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

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Rationale: 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.

Objectives: 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.

Materials and Methods: 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.

Findings: 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.

Conclusions: Greater prenatal PAH exposure was associated with increased weight, fat mass, adipose gene expression and epigenetic changes in progeny.

Original languageEnglish (US)
Article numbere110706
JournalPLoS One
Volume9
Issue number10
DOIs
StatePublished - Oct 27 2014

Fingerprint

Peroxisome Proliferator-Activated Receptors
Methylation
Polycyclic Aromatic Hydrocarbons
Adiposity
adiposity
polycyclic aromatic hydrocarbons
methylation
DNA methylation
DNA Methylation
Gene expression
CCAAT-Enhancer-Binding Proteins
mice
Gene Expression
Fatty Acid Synthases
gene expression
fatty-acid synthase
adiponectin
Fats
Adiponectin
Dams

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

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

In: PLoS One, Vol. 9, No. 10, e110706, 27.10.2014.

Research output: Contribution to journalArticle

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. / Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice. In: PLoS One. 2014 ; Vol. 9, No. 10.
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abstract = "Rationale: 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.Objectives: 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.Materials and Methods: 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.Findings: 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.Conclusions: Greater prenatal PAH exposure was associated with increased weight, fat mass, adipose gene expression and epigenetic changes in progeny.",
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