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

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.
AuthorsAndrew A Bremer, Walter L Miller
JournalFertility and sterility (Fertil Steril) Vol. 89 Issue 5 Pg. 1039-1048 (May 2008) ISSN: 1556-5653 [Electronic] United States
PMID18433749 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
Chemical References
  • Androgens
  • Gonadotropins
  • Steroids
  • Serine
Topics
  • Androgens (blood)
  • Female
  • Gonadotropins (metabolism)
  • Humans
  • Insulin Resistance (physiology)
  • Phosphorylation
  • Polycystic Ovary Syndrome (metabolism, physiopathology)
  • Serine (metabolism)
  • Steroids (metabolism)

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