Human Reproduction, Vol. 16, No. 12, 2552-2556,
December 2001
© 2001 European Society of Human Reproduction and Embryology
Follistatin and activin A serum concentrations in obese and non-obese patients with polycystic ovary syndrome
1 IVF Unit and 2 Institute for Hormone Research, Shaare-Zedek Medical Center, Ben-Gurion University, P.O. Box 3235, Jerusalem, Israel, 3 Oxford Brookes University, Oxford, UK and 4 Fertility Clinic, Lis Maternity Hospital, Tel Aviv University, Tel Aviv, Israel
BACKGROUND: Activin promotes ovarian follicular development, inhibits androgen production and increases FSH and insulin secretion. Follistatin, an activin-binding protein, neutralizes activin bioactivity. Therefore, a decrease in the ratio of activin/follistatin might encourage characteristic features of polycystic ovary syndrome (PCOS). We investigated whether women with PCOS showed disordered follistatin and/or activin serum concentrations. METHODS: The study group included 24 obese and 20 non-obese (body mass index
and <27 kg/m2 respectively) clomiphene-failure PCOS patients. The control group included 16 obese and 46 non-obese patients with normal ovulatory cycles. Blood samples were obtained from the patients on day 35 of a progesterone-induced or spontaneous cycle and were assayed for LH, FSH, testosterone, 17-hydroxy-progesterone, androstenedione, follistatin, activin A, fasting glucose and insulin. RESULTS: Follistatin concentrations were comparable between obese and non-obese PCOS patients (mean ± SE; 1171 ± 103 and 1045 ± 159 pg/ml respectively) and significantly higher than their respective controls (628 ± 61 and 592 ± 49 pg/ml, P < 0.0001 and P < 0.02 respectively). Activin A concentrations were comparable between the four groups (590 ± 35, 513 ± 74, 661 ± 87 and 595 ± 43 pg/ml in obese and non-obese PCOS and controls respectively). Stepwise regression analyses for relationships between follistatin or activin A levels and all other variables indicated that follistatin was significantly and independently positively affected by PCOS (P < 0.0001), age (P < 0.02), androstenedione (P < 0.03) and weight (P < 0.05). Activin A was significantly and independently negatively affected by PCOS (P < 0.003) and FSH (P < 0.03), and positively affected by weight (P < 0.009) and androstenedione (P < 0.02). CONCLUSIONS: Serum follistatin is increased in PCOS patients, regardless of obesity. PCOS is the most significant variable that relates to high follistatin and low activin A serum concentration. A high follistatin/activin ratio could well contribute to the pathophysiology of PCOS.
Key words: activin A/follistatin/obesity/PCOS
5 To whom correspondence should be addressed at: IVF Unit, Shaare-Zedek Medical Center, P.O. Box 3235, Jerusalem 91031, Israel. E-mail: gevat{at}szmc.org.il
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