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Polycystic ovary syndrome is the most common endocrine disorder in women of reproductive
age. Recent prevalence estimates suggest that 5–10% of premenopausal women have the
full-blown syndrome of hyperandrogenism, chronic anovulation, and polycystic ovaries.
Evidence suggests that women with polycystic ovary syndrome have a unique disorder
of insulin action and are at increased risk to develop non-insulin-dependent diabetes
mellitus. Further, non-insulin-dependent diabetes mellitus in women with polycystic
ovary syndrome has a substantially earlier age of onset (third to fourth decades)
than it does in the general population (sixth to seventh decades). Studies assessing
whether abnormalities in insulin action are intrinsic or secondary to the hormonal
milieu have found that insulin-induced receptor autophosphorylation is markedly diminished
in approximately 50% of polycystic ovary syndrome women. This defect is unique to
women with polycystic ovary syndrome and is not seen in other common insulin-resistant
states of obesity and non-insulin-dependent diabetes mellitus. In polycystic ovary
syndrome women who have normal receptor autophosphorylation, it remains likely that
signaling mechanisms downstream of the receptor are abnormal, since these women are
also insulin resistant. This distinctive post-insulin-binding defect appears to be
genetic, since it is present in cells removed from the in vivo environment for generations.
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© 1995 Published by Elsevier Inc.