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Early sex differences in hepatic metabolic signaling in offspring of obese female mice (1033.11)
Author(s) -
Miller Colette,
Krishna Saritha,
Lin Zhoumeng,
DellaFera Mary Anne,
Harn Donald,
Serre Claire,
Baile Clifton,
Filipov Nickolay
Publication year - 2014
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.28.1_supplement.1033.11
Subject(s) - offspring , medicine , endocrinology , biology , lipogenesis , lactation , glut4 , fatty liver , obesity , weaning , fetus , gestation , pregnancy , lipid metabolism , insulin resistance , disease , genetics
Rates of non‐alcoholic fatty liver disease are increasing in all age groups. Maternal obesity imprints the fetal liver; however, little is known about the influence of sex in hepatic metabolic signaling. Thus, the objective of this study was to investigate sex differences in the liver of offspring of high fat diet‐fed (HFD) dams. C57BL/6 dams were fed either a 4.3% or 35% fat diet for 6 weeks prior to and during mating, gestation, and lactation. Offspring were sacrificed at post‐natal day 21 to measure expression of genes related to lipogenesis and insulin signaling. Maternal HFD had a significantly increased offspring body weight (p<0.01). Sex had a significant effect on liver weight (p<0.03) and females from obese dams had smaller livers than both male groups (p<0.10). HFD resulted in 2‐fold increases in the lipogenic transcription factor SREBP1c in both sexes (p<0.02). Sex had a significant effect on GLUT4 expression‐ females having higher expression than males (p<0.05). Furthermore, females from HFD‐fed dams had higher expression of GLUT4 compared to control females (p<0.02). These data show that the liver can be affected by sex and by HFD that is entirely of maternal origin. Grant Funding Source : Support: UGA Obesity Initiative, Atlanta ARCS Fnd, & GRA Eminent Scholar endowment (CAB)