Ontogeny of the ovary in polycystic ovary syndrome

Abstract

Activation of primordial follicles into the growing pool, selection of the dominant follicle, and its eventual ovulation require complex endocrine and metabolic interactions as well as intraovarian paracrine signals to coordinate granulosa cell proliferation, theca cell differentiation, and oocyte maturation. Early preantral follicle development relies mostly upon mesenchymal-epithelial cell interactions, intraovarian paracrine signals, and oocyte-secreted factors, whereas development of the antral follicle depends on circulating gonadotropins as well as locally derived regulators. In women with polycystic ovary syndrome (PCOS), ovarian hyperandrogenism, hyperinsulinemia from insulin resistance, and altered intrafollicular paracrine signaling perturb the activation, survival, growth, and selection of follicles, causing accumulation of small antral follicles within the periphery of the ovary, giving it a polycystic morphology. Altered adipocyte-ovarian interactions further compound these adverse events on follicle development and also can harm the oocyte, particularly in the presence of increased adiposity. Finally, endocrine antecedents of PCOS occur in female infants born to mothers with PCOS, which suggests that interactions between genes and the maternal-fetal hormonal environment may program ovarian function after birth.

Phospholipase C-zeta deficiency as a cause for repetitive oocyte fertilization failure during ovarian stimulation for in vitro fertilization with ICSI: a case report

“…Instead, Ca 2+ ionophore was successful in overcoming PLC-ζ-deficient sperm fertilization failure when used after ICSI of PCOS oocytes matured in vitro, supporting a report of successful pregnancy occurring after ICSI with artificial activation of in vitro matured oocytes [33]. It is possible that androgen-induced impairment of Ca 2+ oscillations in PCOS oocytes matured in vivo reduced the benefit of artificial oocyte activation, without diminishing the value of using Ca 2+ ionophore after ICSI of PCOS oocytes matured in vitro [34][35][36]. The finding that one blastocyst arose from an oocyte stimulated with Ca 2+ -induced activation from a PCOS patient, which led to a term infant female, raises the additional possible benefit of Ca 2+ ionophore on preimplantation embryogenesis.…”

Dual targeting of TNF-αand free radical toxic stress as a promising strategy to manage experimental polycystic ovary

“…Hyperinsulinemia is believed to be a stimulator of hyperandrogenism and chronic oligo-or anovulation (González, 2012). Insulin excess can cause fulliculogenesis disruption through stimulating androgen production by theca cells and elevating serum-free testosterone levels (Dumesic & Richards, 2013).…”

Obesity and PCOS: The Effect of Metabolic Derangements on Endometrial Receptivity at the Time of Implantation

“…[77][78][79] Insulin excess binds to its receptor on the ovarian theca cell, enhancing LH-and IGF-I-stimulated androgen production. 80 Insulin also acts indirectly to increase serum-free testosterone by inhibiting the hepatic production of sex hormone-binding globulin 80,81 and enhances serum IGF-I bioactivity through suppressed IGF-binding protein production, perpetuating ovarian hyperandrogenism. 80 Obesity increases hyperandrogenism, both independently and by exacerbating PCOS.…”