The serine phosphorylation hypothesis of polycystic ovary syndrome: a unifying mechanism for hyperandrogenemia and insulin resistance.
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.
Bremer
Andrew A
AA
Department of Pediatrics, Division of Endocrinology, University of California-Davis, Sacramento, California. Electronic address: andrew.bremer@ucdmc.ucdavis.edu.
Miller
Walter L
WL
Department of Pediatrics, Division of Endocrinology, University of California-San Francisco, San Francisco, California.
D000728:Androgens / Q000097:blood*; D005260:Female; D006062:Gonadotropins / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D010766:Phosphorylation; D011085:Polycystic Ovary Syndrome / Q000378:metabolism* / Q000503:physiopathology; D012694:Serine / Q000378:metabolism*; D013256:Steroids / Q000378:metabolism
D000728:Androgens; D006062:Gonadotropins; D013256:Steroids; D012694:Serine