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Ovarian dysfunction in Polycystic Ovary Syndrome (PCOS)

Polycystic Ovary Syndrome: Current and Emerging Concepts, Page: 95-120
2022
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Book Chapter Description

The polycystic ovary (PCO) is defined by the increased number of subcapsular hyperandrogenic follicles and a tendency towards anovulation. This chapter details current knowledge regarding the morphological and functional defects present in these ovaries. Genome-wide association studies (GWAS) of women with polycystic ovary syndrome (PCOS) have revealed linkage to sites close to genes encoding proteins involved in ovarian function, but the majority have not provided definitive mechanistic explanations. Primordial follicle numbers appear normal but increase upon commencement of growth with enhanced survival creating a stockpiling effect. Much has been learned from prenatally androgenised primate models of PCOS, surplus human ovarian tissue from cryopreserved sections, in vitro cell culture models and the ability to perform microarray on small samples. Impaired folliculogenesis and failure of dominant follicle selection underlie the ovulatory dysfunction of PCOS, but ovulatory status appears to fluctuate. Members of the TGFβ family are strongly implicated both pre- and postnatally in disordered preantral and antral follicular development. Overproduction of androgens by the ovarian theca cells of PCO is intrinsic, and GWAS consistently show linkage to DENND1A, a splice variant of which increases steroidogenesis and is overexpressed in PCOS theca. Insulin resistance is common in PCOS with systemic and local ovarian effects, resulting in alteration of cell metabolism that affects both follicle growth and oocyte health.

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