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2014 Abstracts

Intrauterine Growth Restriction Alters Estrogen Serum Levels and Signaling in Rat Adipose Tissue in a Sex Dependent Manner

Danielle Holliday, University of Utah

Life Sciences

Intrauterine growth restriction (IUGR) induces visceral obesity in adulthood, specifically among males. In male rat offspring, IUGR increases visceral adipose tissue (VAT) over subcutaneous adipose tissue (SAT). VAT and SAT functions are regulated by estrogen signaling, and suppressed estrogen signaling contributes to obesity development. Estrogen signaling is composed of estradiol and estrogen receptor alpha (ERα) and beta (ERβ). Estrogen receptors regulate the expression of several obesity related genes, such as lipoprotein lipase (LPL). However, the effects of IUGR on estrogen serum levels and signaling in the adipose tissue are unknown.

We hypothesize that IUGR will alter estradiol serum levels and ERs content in rat offspring adipose tissue in a sex and depot dependent manner.

IUGR was induced by bilateral uterine artery ligation on gestational day 19 in Sprague Dawley rats. Offspring were killed at weaning and serum, VAT and SAT samples collected. Serum estradiol levels and ERα and ERβ protein abundance were measured.

Results are reported as IUGR as % of sex-matched controls ± SD (*p<0.05). IUGR decreased serum estradiol levels in male offspring (51 ± 24 %*) and had no effect on female estradiol levels. IUGR increased ERα (149.1 ± 52.8 %*) and ERβ (396.8 ± 116.8 %*) content in male SAT, with no effects in male VAT. IUGR did not alter ERα or ERβ protein abundance in SAT and VAT of female offspring.In conclusion, IUGR decreased serum estradiol levels and increased ERα and ERβ protein abundance in SAT in male offspring. We speculate that in the SAT, IUGR upregulates ERs as a compensatory mechanism for the decrease of estradiol serum levels, suggesting overall normal estrogen signaling. However, in the VAT, the lower estradiol levels in combination with no changes in ERs may result in an overall decrease of estrogen signaling, contributing to visceral obesity development.