No single etiologic factor fully explains all the features of PCOS. Excess androgen production is primarily from the ovary. Increased testosterone production by theca cells of polycystic ovaries has been demonstrated. Increased LH secretion by the pituitary gland is consistently demonstrated. It is not clear if this is a primary defect in the GnRH pulse generator or if this is a secondary phenomena. Increased LH stimulation to the theca cells drives increased androgen production.
It is also recognized that women with PCOS, independent of body weight, demonstrate insulin resistance. When carefully studied, most women with PCOS demonstrate hyperinsulinemia. Increased insulin resistance is associated with worsening of the clinical manifestations of PCOS. Insulin acts, along with increased LH secretion, to enhance androgen production from the ovary. Insulin also inhibits hepatic production of sex-hormone binding globulin (SHBG). SHBG is the principle binding protein for testosterone, and decreased SHBG results in increases in the proportion of unbound or free testosterone.
Darkening of skin on back of neck/ underarms
Increased waist circumference compared to hip
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