Follicular arrest in polycystic ovary syndrome is associated with deficient inhibin A and B biosynthesis.
BACKGROUND
Previous studies suggest that inhibin subunit expression is decreased in granulosa cells of women with polycystic ovary syndrome (PCOS).


OBJECTIVE
The objective of this study was to test the hypothesis that inhibin A and inhibin B protein concentrations are also decreased in PCOS follicles.


METHODS
The design was a parallel study.


METHODS
The study was performed at an in vitro fertilization suite.


METHODS
We studied women with regular cycles (n = 36) and women with PCOS (n = 8).


METHODS
Follicular fluid was aspirated from the follicles of women with PCOS (n = 14 follicles) and from women with regular cycles at various times during the follicular phase (n = 50 follicles).


METHODS
Inhibin A and B concentrations from PCOS follicles were compared with those in size-matched follicles, dominant follicles (> or = 10 mm), and subordinate follicles from regularly cycling women.


RESULTS
Inhibin A (220 +/- 38 vs. 400 +/- 72 IU/ml; P < 0.05) and inhibin B (75.4 +/- 10.4 vs. 139 +/- 26 ng/ml; P < 0.05) concentrations were lower in the follicular fluid of PCOS follicles compared with those of size-matched follicles from regularly cycling women. Inhibin A was also lower in the follicular fluid of PCOS compared with subordinate follicles from normal women (577 +/- 166 IU/ml; P < 0.05). Inhibin A concentrations increased with increasing follicle size, resulting in significantly higher follicular fluid concentrations in dominant follicles from normal women compared with PCOS follicles (2298 +/- 228 IU/ml; P < 0.05).


CONCLUSIONS
These data demonstrate that inhibin A and inhibin B concentrations are significantly reduced in the follicular fluid of women with PCOS compared with those in the follicular fluid of size-matched follicles from normal women, consistent with the decreased inhibin subunit mRNA expression in previous studies. These findings point to the potential importance of inhibins in normal follicle development and suggest that inhibin deficiency may play a role in the follicle arrest associated with PCOS.
Welt
Corrine K
CK
Reproductive Endocrine Unit, Department of Medicine, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114, USA. cwelt@partners.org
Taylor
Ann E
AE
Fox
Janis
J
Messerlian
Geralyn M
GM
Adams
Judith M
JM
Schneyer
Alan L
AL
D028341:Activins / Q000378:metabolism; D000293:Adolescent; D000328:Adult; D000735:Androstenedione / Q000097:blood; D015992:Body Mass Index; D004958:Estradiol / Q000097:blood / Q000378:metabolism; D005260:Female; D043373:Follicle Stimulating Hormone, Human / Q000097:blood; D015571:Follicular Fluid / Q000378:metabolism; D006801:Humans; D028322:Inhibin-beta Subunits / Q000378:metabolism; D007265:Inhibins / Q000097:blood / Q000172:deficiency*; D007986:Luteinizing Hormone / Q000097:blood; D006080:Ovarian Follicle / Q000502:physiology*; D011085:Polycystic Ovary Syndrome / Q000473:pathology*; D013739:Testosterone / Q000097:blood
D043373:Follicle Stimulating Hormone, Human; C422405:activin A; C422362:inhibin A; C422364:inhibin B; D028341:Activins; D013739:Testosterone; D000735:Androstenedione; D004958:Estradiol; D007265:Inhibins; D007986:Luteinizing Hormone; D028322:Inhibin-beta Subunits