PCOS Forum

Research in Polycystic Ovary Syndrome Today and Tomorrow

Renato Pasquali; Elisabet Stener-Victorin; Bulent O. Yildiz; Antoni J. Duleba; Kathleen Hoeger; Helen Mason; Roy Homburg; Theresa Hickey; Steve Franks; Juha S. Tapanainen; Adam Balen; David H. Abbott; Evanthia Diamanti-Kandarakis; Richard S. Legro


Clin Endocrinol. 2011;74(4):424-433. 

In This Article

Mechanism of Follicle Arrest

The finding that granulosa cells from anovulatory PCO responded well to FSH in culture directed initial investigations into follicular arrest towards discovery of raised levels of a locally produced inhibitor. It is difficult to deduce cause and effect, however, whether the factor is causing follicular arrest or did the follicular arrest elicit the production of the inhibitor. Androgens are an obvious candidate, but production is raised in theca from ovulatory PCO also.[31] Insulin causes premature acquisition of LH receptors possibly leading to early follicular luteinization,[32] but the insulin signalling defect in the polycystic ovary remains to be clarified. More comprehensive investigation into insulin/glucose interactions in these cells has been undertaken, utilizing a metabolomic approach. Anti-Mullerian hormone (AMH) is raised in women with PCOS, and granulosa cell production is considerably higher in anovulatory than ovulatory women with PCOS. AMH's suppressive effects on folliculogenesis may make this the sought-after local inhibitor.[33] Recent data indicated that it is those women in whom AMH levels fall who have the best response to methods to induce ovulation. Interestingly, the incubation of cells with metformin inhibited AMH production, suggesting that this may be one mechanism of action of this drug in PCOS.[34]


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