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.
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Authors | Andrew A Bremer, Walter L Miller |
Journal | Fertility and sterility
(Fertil Steril)
Vol. 89
Issue 5
Pg. 1039-1048
(May 2008)
ISSN: 1556-5653 [Electronic] United States |
PMID | 18433749
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
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Chemical References |
- Androgens
- Gonadotropins
- Steroids
- Serine
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Topics |
- Androgens
(blood)
- Female
- Gonadotropins
(metabolism)
- Humans
- Insulin Resistance
(physiology)
- Phosphorylation
- Polycystic Ovary Syndrome
(metabolism, physiopathology)
- Serine
(metabolism)
- Steroids
(metabolism)
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