Androgens and polycystic ovary syndrome.
OBJECTIVE
Polycystic ovary syndrome (PCOS) is a common complex endocrine genetic disorder, which involves overproduction of androgens, leading to heterogeneous range of symptoms and associated with increased metabolic and cardiovascular morbidity. This review focuses on androgen biosynthesis, use, metabolism in PCOS and clinical consequences of hyperandrogenism.


RESULTS
Controversial definition of the disorder and different phenotypic subgroups present a challenge for clinical and basic research. Further investigation of different phenotypes highlights the fact that PCOS probably represents a group of disorders with different etiologies. Prenatal androgen exposure and adolescent studies suggest early in life androgen excess as initiating factor of PCOS, but insufficient evidence available to confirm this hypothesis. Various intracellular signaling pathways implicated in PCOS steroidogenesis and in androgen action have been studied, however, PCOS pathogenesis remains obscure. Growing evidence links androgens with pathophysiology of PCOS and metabolic derangements.


CONCLUSIONS
Despite intensive investigation, etiology and underlying mechanisms of PCOS remain unclear, warranting further investigation. Better understanding of molecular and genetic basis might lead to invention of novel therapeutic approaches. Long-term interventional studies that lower androgen levels in women with hyperandrogenism might protect against metabolic and cardiovascular comorbidities are needed.
Nisenblat
Vicki
V
Robinson Institute, School of Pediatrics and Reproductive Health, University of Adelaide, South Australia, Australia.
Norman
Robert J
RJ
D000728:Androgens / Q000378:metabolism*; D000818:Animals; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D011085:Polycystic Ovary Syndrome / Q000150:complications / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012307:Risk Factors; D015398:Signal Transduction; D009626:Terminology as Topic; D013739:Testosterone / Q000378:metabolism*; D015854:Up-Regulation
D000728:Androgens; D013739:Testosterone