Hyperinsulinism and its interaction with hyperandrogenism in polycystic ovary syndrome.
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. It has become increasingly evident that insulin resistance plays a significant role both as a cause and result of the syndrome. The purpose of this review is to summarize the possible mechanisms leading to insulin resistance and resultant hyperinsulinism (HI) and their interaction with hyperandrogenism (HA) in PCOS. We conducted a computerized search of MEDLINE for relevant studies in the English literature published between January 1966 and January 2000. We reviewed all studies that investigated the roles of insulin, insulin receptor, and insulin gene in insulin resistance and its interaction with hyperandrogenism in PCOS. Insulin resistance in PCOS seems to involve a postbinding defect in the insulin receptor and/or in the receptor signal transduction. Current research has focused on identifying a genetic predisposition for insulin resistance in this syndrome. The answer to the question whether HI or HA is the initiating event is still unclear inasmuch as there are clinical and molecular evidences to support both of these approaches. Our view is that whichever is the triggering insult, a vicious cycle is established where HI acts to aggravate HA and vice versa. In this model, obesity and genetic predisposition seem to be the independent factors that can give rise or contribute to HI, HA, or both simultaneously. It seems that "hyperinsulinemic hyperandrogenism" represents a significant subgroup of PCOS, which probably needs to be renamed and reclassified in the light of this new approach.
Sozen
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Owensboro Mercy Hospital, Kentucky, USA.
Arici
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D000818:Animals; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D017588:Hyperandrogenism / Q000150:complications / Q000235:genetics / Q000503:physiopathology*; D006946:Hyperinsulinism / Q000150:complications / Q000235:genetics / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology; D009765:Obesity / Q000150:complications / Q000503:physiopathology; D011085:Polycystic Ovary Syndrome / Q000150:complications / Q000235:genetics / Q000503:physiopathology*; D013739:Testosterone / Q000502:physiology
D013739:Testosterone