Pathophysiology of ovarian steroid secretion in polycystic ovary syndrome

Seminars in Reproductive Endocrinology
R Barnes

Abstract

The ovary in polycystic ovary syndrome (PCOS) produces markedly increased amounts of steroids in response to gonadotropin stimulation. Because FSH secretion is under tight long-loop negative-feedback control and LH is not, hyperandrogenism is the primary clinical manifestation of excess steroid production in PCOS. However, estrogen production by multiple, small follicles may inhibit FSH secretion sufficiently to prevent selection of a single, dominant follicle. Ovarian stimulation testing has suggested that ovarian hyperandrogenism is a result of dysregulation of the androgen producing enzyme P450c17. ACTH stimulation testing is consistent with dysregulation of adrenal P450c17 in about two-thirds of hyperandrogenic women. In most cases dysregulation appears to be due to an intrinsic abnormality of P450c17, or to an abnormality of autocrine/paracrine factors which regulate P450c17. Both LH and insulin hypersecretion are most often a result of the steroid secretory abnormalities. Once present they may amplify the underlying cause of dysregulation of P450c17.

Citations

Jun 1, 2001·Fertility and Sterility·U HeiderK Spanel-Borowski
Mar 10, 2007·PPAR Research·Pascal Froment, Philippe Touraine
Oct 25, 2002·Gynecological Endocrinology : the Official Journal of the International Society of Gynecological Endocrinology·L FalsettiE Sartori
Jul 25, 1998·The European Journal of Contraception & Reproductive Health Care : the Official Journal of the European Society of Contraception·I HalikiasG Tolis
Apr 8, 2006·Fertility and Sterility·Assimina Galli-TsinopoulouSanda Nousia-Arvanitakis
Apr 11, 2001·Obstetrics and Gynecology Clinics of North America·J V ZborowskiJ A Cauley
Nov 12, 2016·Clinica Chimica Acta; International Journal of Clinical Chemistry·Shi-Wen JiangJiayin Liu
Dec 18, 1998·Journal of Endocrinological Investigation·R B Barnes

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