Abstract
Polycystic ovary syndrome (PCOS) seems to arise as a complex trait that results from the interaction of diverse genetic and environmental factors. One of main hypothesis is that PCOS result from functional ovarian hyperandrogenism (FOH) due to dysregulation of androgen secretion. There is a contribution of adrenal androgens like DHEA, that are metabolized in the ovary to androstenedione and the testosterone. Heritable factors include PCOM, hyperandrogenemia, insulin resistance, and insulin secretory defects. Environmental factors include prenatal androgen exposure and poor fetal growth, whereas acquired obesity is a major postnatal factor. A metabolic syndrome of obesity-related and/or intrinsic insulin resistance occurs in about half of PCOS patients, and the compensatory hyperinsulinism has tissue-selective effects, which include aggravation off hyperandrogenism. The variety of pathways involved and lack of a common thread attests to the multifactorial nature and heterogeneity of the syndrome. Knowing the fundamental basis of the disorder is necessary to optimally correct androgen levels, ovulation, and metabolic homeostasis, and solve the Ob & Gyn problems as well.
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