MON-192 Gestational exposure to excess testosterone disrupts maternal steroid homeostasis and perturbs the steroid-lipid association in sheep
Abstract
Abstract Disclosure: N. Saadat: None. R. Saeed: None. B. Pallas: None. A.K. Vyas: None. R.J. Auchus: None. V. Padmanabhan: None. Steroid hormones play a key role in pregnancy and in the growth and development of the fetus. Hyperandrogenism during pregnancy may disrupt this steroid homeostatic balance leading to unfavorable metabolic profiles, pregnancy complications and adverse programming for diseases later in life of the offspring. We hypothesized that gestational exposure of excess testosterone will not only disrupt maternal steroid homeostasis but also perturb the steroid-lipid relationship. Using a well-established translationally relevant sheep model, we investigated the impact of gestational testosterone (T) excess on maternal delta 4 and delta 5 steroid panels and steroid-lipidome relationship at day 127.1 ± 5.3 of pregnancy (term 147 days) in T-treated (T =12, 100mg T-propionate in corn oil, days 30 to 90 of gestation twice weekly intramuscularly) and control (C =5, vehicle only) Suffolk sheep. Steroids were measured using liquid chromatography-tandem mass spectrometry and lipids by shotgun lipidomics. Principal component analysis showed a clear separation of steroid profiles of T-treated and C groups. The main impact of gestational T excess was on the delta 5 pathway, reflected as significant reduction in 17-OH pregnenolone, androstenediol, allopregnanolone, and androsterone, and a reduced trend in dehydroepiandrosterone (DHEA, p=0.08) and 17-OH allopregnanolone…
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