Serum levels of inhibins are differentially altered in patients with polycystic ovary syndrome: effects of being overweight and relevance to hyperandrogenism.
OBJECTIVE
To explore the abnormalities of serum inhibin isoform concentrations in a large group of patients with polycystic ovary syndrome (PCOS) and to evaluate the influence of body mass index (BMI), age, LH, and androgens on serum inhibin levels.


METHODS
Prospective study.


METHODS
Reproductive endocrinology unit of an academic medical center.


METHODS
Forty-one women with PCOS were compared with 24 healthy women.


METHODS
Blood sampling was performed in the early follicular phase in patients and in control women.


METHODS
Serum levels of inhibin A, inhibin B, alpha-inhibin, pro-alphaC (alpha-inhibin precursor proteins), LH, FSH, E(2), T, and androstenedione (A) were assessed in all subjects.


RESULTS
Serum alpha-inhibin levels together with LH, T, and A levels were significantly increased in women with PCOS. Serum inhibin A levels were lower in patients with PCOS than controls (median +/- SD: 7.35 +/- 2.9 vs. 9.4 +/- 4.7 pg/mL), pro-alphaC levels were higher (264 +/- 136.7 vs. 127 +/- 81.5 pg/mL), and inhibin B levels did not differ between the groups (110.5 +/- 51.5 vs. 108 +/- 47.5 pg/mL). Simple regression analysis showed that inhibin A and B levels were negatively correlated with BMI in patients with PCOS (r = -0.43 and r27 kg/m(2)) displayed significantly lower inhibin A and inhibin B levels and a higher pro-alphaC-inhibin A ratio than nonobese patients with PCOS (BMI </=27 kg/m(2)). In this last subgroup, the mean inhibin B level was significantly higher than in controls (median +/- SD: 144 +/- 53.5 vs. 108 +/- 47.5 pg/mL). Partial regression analysis, after controlling for age and BMI, demonstrated that in patients with PCOS, pro-alphaC levels were positively and independently correlated with LH and A levels.


CONCLUSIONS
Among women with PCOS, the trend toward an excess serum inhibin B level is observed exclusively in nonobese patients. The higher pro-alphaC levels and the lower inhibin A levels might reflect a defect in the processing of inhibins specific to polycystic ovaries. In addition, our data suggest that pro-alphaC originates from the theca-interstitial cells and could participate in control of the androgen production by these cells.
Pigny
P
P
Clinique Marc Linquette, Centre Hospitalier Régional Universitaire; and Centre d'Etude et de Recherche en Informatique Médicale, Faculté de Médecine Henri Warembourg, Lille, France.
Cortet-Rudelli
C
C
Decanter
C
C
Deroubaix
D
D
Soudan
B
B
Duhamel
A
A
Dewailly
D
D
D000293:Adolescent; D000328:Adult; D000735:Androstenedione / Q000097:blood; D015992:Body Mass Index; D004958:Estradiol / Q000097:blood; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000150:complications*; D007265:Inhibins / Q000097:blood*; D007986:Luteinizing Hormone / Q000097:blood; D009765:Obesity / Q000150:complications*; D011085:Polycystic Ovary Syndrome / Q000097:blood* / Q000150:complications; D011498:Protein Precursors / Q000097:blood; D013739:Testosterone / Q000097:blood
D011498:Protein Precursors; C095971:inhibin-alpha subunit precursor; D013739:Testosterone; D000735:Androstenedione; D004958:Estradiol; D007265:Inhibins; D007986:Luteinizing Hormone