The serine phosphorylation hypothesis of polycystic ovary syndrome: a unifying mechanism for hyperandrogenemia and insulin resistance

Andrew A. Bremer, Walter L. Miller

Research output: Contribution to journalArticle

61 Scopus citations

Abstract

Polycystic ovary syndrome (PCOS) is a common endocrinopathy affecting 4%-8% of reproductive-aged women. The syndrome is characterized by hyperandrogenemia and disordered gonadotropin secretion and is often associated with insulin resistance. However, rather than being one disease entity caused by a single molecular defect, PCOS under its current diagnostic criteria most likely includes a number of distinct disease processes with similar clinical phenotypes but different pathophysiologic mechanisms. The serine phosphorylation hypothesis can potentially explain two major features of PCOS-hyperandrogenemia and insulin resistance. Further defining the molecular mechanisms regulating androgen biosynthesis and insulin action in PCOS patients will permit a better understanding of the syndrome and may lead to the generation of novel specific pharmacologic therapies.

Original languageEnglish (US)
Pages (from-to)1039-1048
Number of pages10
JournalFertility and Sterility
Volume89
Issue number5
DOIs
StatePublished - May 2008

Keywords

  • hyperandrogenemia
  • insulin resistance
  • Polycystic ovary syndrome
  • serine phosphorylation
  • steroidogenesis

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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