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Exercise during pregnancy attenuates prenatal high‐fat diet‐induced hypermethylation of the Pgc‐1α gene and protects against age‐induced glucose intolerance in the offspring
Author(s) -
Laker Rhianna Che,
Lillard Travis,
Okutsu Mitsuhara,
Connelly Jessica,
Yan Zhen
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1134.3
Subject(s) - offspring , endocrinology , medicine , pregnancy , dna methylation , biology , epigenetics , fetus , overnutrition , obesity , metabolic syndrome , litter , gene expression , gene , genetics , agronomy
Maternal obesity predisposes the fetus to metabolic disease later in life. We determined whether maternal diet and exercise impose epigenetic influences in offspring on a metabolic master regulator, peroxisome proliferator activated receptor γ co‐activator 1α (Pgc‐1α). Female C57BL6 mice were exposed to either normal chow, high‐fat diet (HFD), or voluntary wheel running exercise with HFD for 6 wks prior to and throughout pregnancy. Genomic DNA from skeletal muscle was isolated from neonatal offspring for DNA methylation analysis of the Pgc‐1α promoter using pyro‐sequencing. Litter size and offspring weight were not different between groups. Pgc‐1α methylation of CpG ‐260, a site shown to be associated with metabolic disease in humans, was increased (P<0.05) in offspring skeletal muscle when exposed to maternal HFD. The adult offspring of high‐fat fed mothers displayed impaired glucose tolerance and insulin sensitivity in later life. Maternal exercise attenuated the maternal HFD‐induced hypermethylation at birth and protected adult offspring from age‐related decline in metabolic function. Funded by the Partners’ Fund from the Robert M. Berne Cardiovascular Research Center and Thelma R. Swortzel Award, University of Virginia.