Abstract
BackgroundThe influence of estradiol (E2) on granulosa cell (GC) function has not been tested clinically in women with polycystic ovary syndrome (PCOS). The objective of this study is to determine if E2 influences GC responses to FSH in women with PCOS.MethodsThis is a two phase, single cohort study conducted over a 2-year period at a single academic center. Nine women with PCOS according to NIH criteria. In Phase 1, FSH stimulation of GC responses as measured by E2 and Inhibin B (Inh B) were assessed before and at 5 and 6 weeks after GnRH agonist administration. In Phase 2, the same protocol was employed with the addition of an aromatase inhibitor (letrozole, LET) administered daily beginning at week 4 for 2 weeks.ResultsIn Phase 1, recovery of FSH, E2 and Inh B from ovarian suppression occurred at 5 and 6 weeks after GnRH agonist injection and preceded resumption of LH and androgen secretion. In Phase 2, hormone recovery after GnRH agonist was characterized by elevated FSH and suppressed E2 levels whereas recovery of LH and androgen levels were unchanged. In Phase 1, FSH stimulated E2 and Inh B responses were unaltered during recovery from ovarian suppression. In Phase 2, E2 and Inh B fold changes after FSH were significantly reduced at weeks 5 (p < 0.04) and 6 (p < 0.01), respectively.ConclusionIn anovulatory women with PCOS, chronic, unopposed E2 secretion may contribute, at least in part, to enhanced ovarian responsiveness to FSH.Trial registrationNCT02389088
Highlights
The influence of estradiol (E2) on granulosa cell (GC) function has not been tested clinically in women with polycystic ovary syndrome (PCOS)
In vitro and in vivo studies have demonstrated that granulosa cells (GCs) from women with PCOS are hyperresponsive to FSH stimulation compared to responses observed in normal GCs
We and others have shown that in women with PCOS serum E2 and inhibin B (Inh B) exhibit similar temporal responsiveness to FSH [11, 12]. These findings suggest that Inhibin B (Inh B) may serve as a marker of granulosa cell activity alongside E2
Summary
The influence of estradiol (E2) on granulosa cell (GC) function has not been tested clinically in women with polycystic ovary syndrome (PCOS). The objective of this study is to determine if E2 influences GC responses to FSH in women with PCOS. Local production of E2 may account, at least in part, for the enhanced CG response to FSH in PCOS. There is considerable evidence that estrogen enhances follicle function including responses to FSH. Diethylstilbestrol treated GCs from immature hypophysectomized rats produced greater E2 release in response to FSH compared to that of untreated cells [4]. Synergy between E2 and FSH has been demonstrated in GCs with regards to increased FSH receptor binding and increased aromatase activity [8,9,10].
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