Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 38 P141 | DOI: 10.1530/endoabs.38.P141

SFEBES2015 Poster Presentations Growth and development (5 abstracts)

Inter-correlations between placental genes regulating foetal glucocorticoid exposure and IGF2 in maternal severe obesity: a mechanism for higher birthweight?

Theresia Mina 1, , Simon Riley 2, , Jane Norman 2, & Rebecca Reynolds 1,

1BHF Centre for Cardiovascular Sciences, QMRI, The University of Edinburgh, Edinburgh, UK; 2MRC Centre for Reproductive Health, QMRI, The University of Edinburgh, Edinburgh, UK; 3Tommy’s Centre for Maternal and Fetal Health, QMRI, The University of Edinburgh, Edinburgh, UK.

Background: Maternal obesity in pregnancy associates with higher birthweight. A key pathway is through placental regulation of hormones controlling foetal growth. As excess foetal glucocorticoid exposure associates with lower birthweight and since placental Insulin-like Growth Factor (IGF2) may be modulated by glucocorticoids, we hypothesised that the expression profiles of placental genes leading to reduced glucocorticoid exposure and increased IGF2 mRNA level correlate with higher birthweight in severely obese pregnancy.

Methods: The mRNA levels of placental genes regulating glucocorticoid synthesis (11β-HSD1), clearance (11β-HSD2), sensitivity (NR3C1-αIGF2 and IGF2R were quantified in term placental samples from lean (BMI ≤ 25 kg/m2, n=42) and very severely obese (SO BMI ≧ 40 kg/m2, n=43) pregnancies exclusive of antenatal steroids and gestational diabetes. Neonatal anthropometry was obtained from hospital records. Ethical approval was obtained.

Results: The standardised (SDS) birthweight, SDS birth length, SDS BMI and all mRNA levels were similar in both groups. In SO placentas only, mRNA levels of 11β-HSD1 and NR3C1-α positively correlated with IGF2 and IGF2R (all ρ<0.30, p<0.05). Higher placental 11β-HSD1 (ρ=0.29, P=0.09), NR3C1-α (ρ=0.54, P=0.001), and lower 11β-HSD2 (ρ=0.42, P=0.012) mRNAs (consistent with increased foetal glucocorticoid exposure) correlated with shorter birth length in lean only. Higher placental 11β-HSD1 (ρ=0.35, P=0.04) and NR3C1-α? (ρ=0.35, P=0.04) also correlated with increased SDS BMI in lean only. None of the genes correlated with SDS birthweight in lean. Only in SO group did we observe correlations between increased placental IGF2 mRNA and higher SDS birthweight (ρ=0.40, P=0.005).

Discussion: The inter-correlations between glucocorticoid-linked genes with IGF2 and IGF2R in SO placentas, but not in controls, support a modulatory role of glucocorticoids on placental foetal growth through excess IGF2 exposure in foetuses of SO pregnancy. Further, the contrasting correlation profiles of placental gene expression and infant’s size at birth between lean and SO group suggest a protective-adaptive response in SO placentas that prevent growth restriction and support excess birthweight.

Volume 38

Society for Endocrinology BES 2015

Edinburgh, UK
02 Nov 2015 - 04 Nov 2015

Society for Endocrinology 

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