CONICET | Buscador de Institutos y Recursos Humanos

An adverse environment during prenatal life programs the developing embryo and may conduct to diseases during the adult life. Prenatal hyperandrogenism is able to induce endocrine and metabolic abnormalities, mimicking those observed in human polycystic ovary syndrome (PCOS) phenotypes. The aim of this work is to evaluate the effect of prenatal hyperandrogenism on lipid and metabolic balance and its impact on ovarian steroidogenesis.Pregnant rats were hyperandrogenized with testosterone and a Control (Ctl) group was obtained by vehicle injection. The prenatally hyperandrogenized (PH) female offspring and Ctl offspring were characterized according to the estrous cycle as ovulatory (PHov) and anovulatory (PHanov) phenotypes. To evaluate the effect of androgen excess on general lipid metabolism we measured growth rate curve and serum lipid profile. As the liver is a major metabolic regulatory organ we evaluated liver triglycerides content and the mRNA levels by qPCR of key factors involved in lipogenesis. To study the impact of prenatal hyperandrogenism on ovarian functions we evaluated ovarian histology, testosterone and estradiol serum levels. We quantified by qPCR the mRNA levels of PPARg and its co-activator PGC1a (a master regulator of lipid metabolism which is also involved in the regulation of steroidogenesis) and steroidogenic enzymes.Ctl rats showed (100%) regular estrous cycles. PH group showed: 43?51% of irregular estrous cycles (PHov), whereas 27?39% presented anovulatory cycles (PHanov). None of the groups displayed body weight differences. Both PH groups presented an increased risk of metabolic syndrome. Although neither PH groups showed signs of liver lipid content, lipogenesis factors were increased. Both PH groups also displayed high levels of serum testosterone and alterations in ovarian morphology, with cysts. Estradiol levels were only decreased in PHanov (p