Current concepts in the polycystic ovary syndrome

A. Dunaif*, A. Thomas

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

274 Scopus citations


Over the past 20 years, it has been clearly documented that the polycystic ovary syndrome (PCOS) has major metabolic sequelae related to insulin resistance and that insulin resistance plays an important role in the pathogenesis of the reproductive disturbances of the disorder. Family studies have indicated a genetic susceptibility to PCOS. Polycystic ovaries and hyperandrogenemia are present in ∼50% of sisters of affected women. Increased androgen secretion and insulin resistance persist in cultured theca cells and skin fibroblasts, respectively, from women with PCOS; this finding suggests that these are intrinsic, presumably genetic, defects. Insulin resistance and elevated low-density lipoprotein (LDL) levels also cluster in the sisters of women with PCOS, consistent with genetic traits. Moreover, the brothers of women with PCOS have insulin resistance and elevated dehydroepiandrosterone sulfate (DHEAS) levels, which supports a genetic basis for these findings. Family-based studies of linkage and association have implicated several genes in the pathogenesis of PCOS. The strongest evidence to date points to a gene in the region of the insulin receptor. Insulin-sensitizing therapy mitigates the reproductive disturbances of PCOS.

Original languageEnglish (US)
Pages (from-to)401-419
Number of pages19
JournalAnnual review of medicine
StatePublished - Mar 17 2001


  • Androgens
  • Diabetes mellitus
  • Genetics
  • Insulin resistance
  • Polycystic ovaries

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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