PCOS begins with hyperinsulinemia in patients, typically those who are insulin- resistant. Through an unknown mechanism, the excess insulin leads to increased GnRH pulse frequency from the hypothalamus.
Abnormal GnRH release in PCOS influences the anterior pituitary to release LH in large amounts.
FSH levels stay normal or decrease by a small amount. These levels would normally increase, however there is LH over FSH dominance, which allows LH to increase in this disorder (estrogen inhibits FSH, but anovulation increases LH).
Due to increased levels of LH, theca-lutein cells begin to increase androgen production, (androstenedione). Through a few conversion steps, this is typically converted to estrogen. However, there is so much androgen production, that a large amount of it is not converted.
High levels of insulin and testosterone decrease levels of steroid hormone-binding globulin (SHBG). Typically, SHBG binds to testosterone, making it less active in the bloodstream. As these SHBGs decrease, testosterone becomes more physiologically active, as there is more free testosterone available.
Due to aromatase in fat cells, patients who are obese also have increased estrogen levels. This occurs because aromatase converts androgens to estrogen.
As these patients have ovarian cycle disorder, there is no cyclic secretion of estrogen and progesterone. Instead, these patients (the obese ones) have excess unopposed estrogen. This influences the endometrium to proliferate unchecked, and can lead to endometrial cancer.
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