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Exercise ancestry decreases lipogenesis‐related gene expression in skeletal muscle of male offspring
Author(s) -
Guth Lisa M.,
Ludlow Andrew T.,
Witkowski Sarah,
Marshall Mallory R.,
Lima Laila,
Venezia Andrew C.,
Xiao Tao,
Lee MeiLing Ting,
Spangenburg Espen E.,
Roth Stephen M.
Publication year - 2011
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.25.1_supplement.862.3
Subject(s) - offspring , sed , endocrinology , biology , lipogenesis , medicine , gene expression , ex vivo , downregulation and upregulation , andrology , gene , pregnancy , genetics , adipose tissue , in vitro
The study objective was to examine the influence of exercise (EX) ancestry compared to sedentary (SED) ancestry on offspring skeletal muscle gene expression. C57/Bl6 mice (F0) were exposed to EX (wheel running, N=20) or a SED condition (no wheel access, N=20) for 12 weeks prior to breeding. EX males and EX females, and SED males and SED females were bred to produce F1 pups. F0 EX mice had continued access to the wheel during breeding, pregnancy, and weaning. F1 pups were sacrificed at 8 wk without direct exercise exposure. Microarray analysis of gene expression was performed on pooled gastrocnemius RNA from F1 males of each ancestry (5 animals per array; 4 total arrays). After processing the microarray data to minimize false positives, 109 transcripts were differentially expressed between F1 EX and F1 SED. Three targets identified as upregulated in F1 SED offspring have been previously associated with lipogenesis and were selected for real‐time PCR validation ( Adipoq , Scd1 , and Cidec ). Adipoq and Scd1 were verified as significantly upregulated in F1 SED offspring ( p < 0.05) and Cidec tended to be upregulated in F1 SED offspring ( p = 0.06 ) . These preliminary findings indicate that exercise ancestry (i.e., parental exercise stimulus) can affect lipogenesis‐related skeletal muscle gene expression in male mouse offspring. Supported by the UMD School of Public Health Research Seed Money Program and NIH AG000268.