Reproduction Abstracts

The ‘old’ science base generally casts androgens as ‘bad’ for folliculogenesis: agents of follicular atresia and directly involved in reproductive pathologies such as PCOS. A more recent literature has mapped cellular sites of androgen formation and action within the ovarian follicle, pinpointing theca as the source and granulosa its target. Molecular studies have located the androgen receptor (AR) to granulosa cells, functionally coupled to FSH-regulated (cAMP-mediated) gene expression. Experiments show an initial capacity of androgen to enhance FSH action, which is lost or becomes suppressive as follicles mature. Granuolsa cell AR levels decline in the preovulatory follicle, possibly as a protective device against over-sensitisation to FSH. This may be a mechanism for supporting follicular dominance and determining which follicles ovulate. AR knockout studies in mice confirm that androgens regulate follicle progression from pre-antral into the antral stage and benefit oogenesis. Thus androgens are neither good nor bad for folliculogenesis: simply essential. Successful clinical ovarian stimulation regimes take account of this reality.