Session: SAT 532-553-Hyperandrogenic Disorders
Poster Board SAT-551
Experiment 1: Placental samples from 38 women with PCOS and 40 controls, who delivered between gestational week 34 and 42, were collected. The gene expression of steroid receptors (AR and ESR1), steroidogenic enzymes (CYP11A1, HSD3B1, CYP19A1, SRD5A2, AKR1C2, AKR1C3 and HSD11B1) and molecules related to metabolic pathways (ADIPOQ, ADIPOR1, ADIPOR2, IGF1, LEP, LEPR and SCL2A4) were analyzed by TaqMan© low-density array.
Experiment 2: Pregnant rats were daily injected (sc) with 5.0 mg of testosterone propionate (T-treated; n=8) or sesame oil (control; n=7) from GD15 until GD19. Placentas were collected on GD21 to measure total and phosphorylated protein expression of eukaryotic initiation factor 4E binding protein 1 (4E-BP1), S6 ribosomal protein and signal transducer and activator of transcription 3 (STAT-3) by western blot, which are known to regulate placental amino acid transporters.
Results: The placental mRNA expression of ESR1 (P = 0.015) and AKR1C3 (P = 0.023) were higher and CYP11A1 (P = 0.024), LEP (P = 0.005), LEPR (P = 0.023) and SCL2A4 (P < 0.001) were lower in women with PCOS compared to controls. These genes encode for ERα, 17β-HSD5, P450scc, leptin, leptin receptor and GLUT4, respectively. mTOR activity was unaltered in the placenta from T-treated rats. Total and phosphorylated STAT3, which is downstream of the leptin receptor, remain to be analyzed.
Conclusion: Increased placental expression of ERα and steroidogenic enzymes (17β-HSD2/5) were observed in women with PCOS similar to reported in androgenized pregnant rats. Moreover, our preliminary data suggest that placental leptin signaling is inhibited in PCOS. Because leptin stimulates placental amino acid transport, these changes could lead to altered transport of nutrients to the fetus.
Nothing to Disclose: MM, IS, EV, H, SS, MS, TJ, ES
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