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The serine phosphorylation hypothesis of polycystic ovary syndrome: a unifying mechanism for hyperandrogenemia and insulin resistance.
Fertil Steril 2008; 89(5):1039-48FS

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.

Authors+Show Affiliations

Department of Pediatrics, Division of Endocrinology, University of California-Davis, Sacramento, California 95817-2208, USA. andrew.bremer@ucdmc.ucdavis.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

18433749

Citation

Bremer, Andrew A., and Walter L. Miller. "The Serine Phosphorylation Hypothesis of Polycystic Ovary Syndrome: a Unifying Mechanism for Hyperandrogenemia and Insulin Resistance." Fertility and Sterility, vol. 89, no. 5, 2008, pp. 1039-48.
Bremer AA, Miller WL. The serine phosphorylation hypothesis of polycystic ovary syndrome: a unifying mechanism for hyperandrogenemia and insulin resistance. Fertil Steril. 2008;89(5):1039-48.
Bremer, A. A., & Miller, W. L. (2008). The serine phosphorylation hypothesis of polycystic ovary syndrome: a unifying mechanism for hyperandrogenemia and insulin resistance. Fertility and Sterility, 89(5), pp. 1039-48. doi:10.1016/j.fertnstert.2008.02.091.
Bremer AA, Miller WL. The Serine Phosphorylation Hypothesis of Polycystic Ovary Syndrome: a Unifying Mechanism for Hyperandrogenemia and Insulin Resistance. Fertil Steril. 2008;89(5):1039-48. PubMed PMID: 18433749.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The serine phosphorylation hypothesis of polycystic ovary syndrome: a unifying mechanism for hyperandrogenemia and insulin resistance. AU - Bremer,Andrew A, AU - Miller,Walter L, Y1 - 2008/04/23/ PY - 2007/09/28/received PY - 2007/12/20/revised PY - 2008/02/07/accepted PY - 2008/4/25/pubmed PY - 2008/6/14/medline PY - 2008/4/25/entrez SP - 1039 EP - 48 JF - Fertility and sterility JO - Fertil. Steril. VL - 89 IS - 5 N2 - 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. SN - 1556-5653 UR - https://www.unboundmedicine.com/medline/citation/18433749/The_serine_phosphorylation_hypothesis_of_polycystic_ovary_syndrome:_a_unifying_mechanism_for_hyperandrogenemia_and_insulin_resistance_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0015-0282(08)00358-0 DB - PRIME DP - Unbound Medicine ER -