Decoding androgen excess in polycystic ovary syndrome: Roles of insulin resistance and other key intraovarian and systemic factors

Figure 5 Intraovarian and systemic factors play a role in disrupting folliculogenesis in polycystic ovary syndrome, resulting in altered steroidogenesis. Heightened luteinizing hormone, insulin resistance, and obesity stimulate theca cell androgen production, while granulosa cell dysfunction impairs aromatization of androgens to estrogens. This hormonal imbalance leads to irregular or absent selection of a dominant follicle, resulting in the persistence of small antral follicles, leading to the characteristic polycystic ovarian morphology. Hyperandrogenism further amplifies the arrest of follicular development, resulting in a vicious cycle of anovulation and hormonal imbalance. LH: Luteinizing hormone; FSH: Follicle-stimulating hormone; PCOM: Polycystic ovarian morphology.