CONICET | Buscador de Institutos y Recursos Humanos

Fetal programming caused by prenatal hyperandrogenism is hypothesized as one of the main factors contributing to polycystic ovary syndrome (PCOS). PCOS is an endocrine-metabolic disorder. Adipokines are involved in metabolic disturbances and also in fertility issues. We aimed to characterize in a PCOS murine model the ovarian secretion pattern of the adipokines Leptin (Lp), Adiponectin (Ad) and Chemerin (Ch) and the consequences on ovarian functions. Pregnants rats were hyperandrogenized with testosterone and a control group was obtained by the injection of vehicle. The prenatally hyperandrogenized (PH) female offspring (N= 150) and control offspring (C, N= 96) were characterized according to the estrous cycle as ovulatory (PHo) and anovulatory (PHa) phenotypes at pubertal age. We evaluate ovarian histology. The adipokine secretion pattern and StAR (the limiting enzyme of steroidogenesis) gene expression were quantified by qPCR. All the groups did not display body weight differences (p > 0.05). In the three independent repetitions of the animal procedure,C rats showed (100%) regular estrous cycle. Within the PH group, 43?51% showed irregular estrous cycles and were considered as PHo, whereas 27?39% presented anovulatory cycles and were considered PHa. Histological examination of ovaries from the PH offspring revealed the presence of cysts and an excess of small antral follicles. The adipokine secretion pattern was altered in the PH groups. Lp levels were lower in PHa group than in C and PHo (po 􀀊p􀀞􀀒.􀀒􀀓􀀋. Ad levels􀁙ere higher in the 􀀲Ho than in C and 􀀲Ha 􀀊p􀀞􀀒.􀀒􀀓􀀋. Ch levels 􀁙ereincreased in the 􀀲Ho vs C and 􀀲Ha 􀀊p􀀞􀀒.􀀒􀀗􀀋. StA􀀴 secretion 􀁙asonly altered in the 􀀲Ha group being higher than in both, C and 􀀲Hogroups 􀀊p􀀞􀀒.􀀒􀀗􀀋. 􀀫n conclusion, fetal programming causes alterationsin ovarian adipo􀁍ines 􀁙ithout the presence of over􀁙eight. The differentiallyderegulation of these adipo􀁍ines is involved in the ovarianalterations displayed in 􀀲C􀀱S phenotypes.