Pathophysiology of ovarian steroid secretion in polycystic ovary syndrome

Randall B. Barnes*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)159-168
Number of pages10
JournalSeminars in reproductive endocrinology
Volume15
Issue number2
DOIs
StatePublished - 1997

Keywords

  • P450c17
  • Polycystic ovary syndrome
  • ovarian hyperandrogenism

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Reproductive Medicine
  • Endocrinology

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