Hum. Reprod. Advance Access published online on February 12, 2004
Human Reproduction, doi:10.1093/humrep/deh145
© 2004 by European Society of Human Reproduction and Embryology
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1 Department of Obstetrics and Gynecology, Università Cattolica del Sacro Cuore, Largo ‘A.Gemelli’ 8, 00168 Roma, Italy; Istituto Scientifico Internazionale Paolo VI, Troina, Italy
* To whom correspondence should be addressed. E-mail: maurizioguido{at}libero.it.
BACKGROUND: To investigate the effect of pioglitazone on adrenal steroidogenesis in polycystic ovary syndrome (PCOS), we studied 11 obese (two with BMI >25 kg/m2; nine with BMI >27 kg/m2) PCOS women before and after 6 months of treatment at a dose of 45 mg/day. METHODS: During the early follicular phase, ultrasonography and hormonal assays were performed. On separate days, all women underwent an oral glucose tolerance test (OGTT), a euglycaemic hyperinsulinaemic clamp and an adrenocorticotrophin hormone (ACTH) test. The same protocol was repeated after therapy. RESULTS: Pioglitazone treatment significantly reduced the insulin response to OGTT and improved the insulin sensitivity indices (P < 0.01 and P = 0.03 respectively). A significant decrease was found in LH (P < 0.05) and androstenedione (P < 0.01) levels after therapy, whereas the other hormonal parameters improved but not significantly. Pioglitazone administration reduced the response of 17 Key words:
Key words: adrenal glands/insulin/PCOS/pioglitazone
Accepted November 28, 2003
Article
Effect of pioglitazone treatment on the adrenal androgen response to corticotrophin in obese patients with polycystic ovary syndrome
2 Department of Obstetrics and Gynecology, Università Cattolica del Sacro Cuore, Largo ‘A.Gemelli’ 8, 00168 Roma, Italy
3 Istituto Scientifico Internazionale Paolo VI, Troina, Italy; OASI Institute for Research, Troina, Italy
Abstract 
-hydroxyprogesterone (17OHP) and androstenedione to ACTH (P < 0.01 and P < 0.02 respectively), most likely through an inhibition of cytocrome P450. The same treatment was able to rebalance the relative activity of 17,20-lyase, as documented by an increase in the androstenedione:17OHP ratio (P < 0.05) after ACTH stimulation. CONCLUSIONS: Our data support the contention that insulin enhances ACTH-stimulated steroidogenesis, while inducing a relative impairment of 17,20-lyase activity. Whether the beneficial effects of pioglitazone on this imbalance could be related to the ameliorated glyco-insulinaemic metabolism or to a direct effect on the adrenal glands remains to be determined.
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