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Maternal pre‐gravid body mass index and adiposity influence umbilical cord gene expression at term in AGA infants
Author(s) -
Thakali Keshari,
Saben Jessica,
Andres Aline,
Shankar Kartik
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.109.3
Subject(s) - endocrinology , medicine , gestational diabetes , overweight , offspring , body mass index , umbilical cord , insulin resistance , obesity , biology , pregnancy , gestation , immunology , genetics
While maternal obesity is associated with unfavorable maternal and fetal outcomes, the influence of maternal obesity on fetal gene expression is less clear. Umbilical cords (UC) from 12 lean (pre‐gravid BMI < 25) and 10 overweight/obese (OB, pre‐gravid BMI ≥25) women without gestational diabetes were collected at term and utilized for gene expression analysis using Human Primeview microarrays (Affymetrix). Although offspring birth weight and infant adiposity (at 2‐wk) did not differ between groups, expression of 232 transcripts was affected in UC from OB compared to lean mothers. GSEA analysis revealed an up‐regulation of genes related to metabolism, stimulus and defense response and inhibitory to insulin signaling in the OB group. We confirmed that Egr‐1, periostin, FosB, and NEDD9 mRNA expression was induced in UCs from OB moms, while endothelin receptor B, Klf10, Peg3 and Egln3 expression was decreased. mRNA expression of Egr‐1, FosB, MEST and SOCS1 was positively associated (p<0.05) with mother's 1 st trimester body fat mass (%). Metabolic and hormonal assessments were also assayed in mother's serum at 30 weeks of gestation and in UC plasma. Our data indicate that maternal obesity per se causes changes in UC gene expression favoring inflammation and insulin resistance, possibly predisposing infants of overweight moms to become overweight later on in life. Funding USDA ARS‐CRIS 6251–51000‐007–04S.