Estimates of incidence of this disorder range around the five percent level if both cessation of ovulation and excess hair growth are used in the definition, but they can range over 10 percent in some select populations. Past research emphasized the relative roles of neuroendocrine abnormalities leading to persistent and excessive secretion of luteinizing hormones (LH), one of two glycoprotein hormones that stimulate the final ripening of the follicles and the secretion of progesterone; and the ovarian actions increased insulin in plasma, a consequence of insulin resistance. Additional evidence suggests that unnatural ovarian production of hormonal steroids is a primary abnormality in PCOS.
Human studies of PCOS have found abnormal ovarian steroid responses to administration of gonadial hormones, specifically potent gonadotropin-releasing hormone (GnRH) agonist or a high dose of human chorionic gonadotropin (hCG). The stimuli cause exaggerated secretion of 17-hydroxyprogesterone (17-OHP) and, to a lesser degree, androstenedione, suggesting abnormal ovarian production of steroids. However, these paradigms involve pharmacological ovarian stimulation and do not reproduce physiological LH pulsatility.
Researchers recently hypothesized that near-physiological LH stimuli would effect greater ovarian secretion of androgens and their precursors in women with PCOS compared to controls. To test this supposition, they employe
Contact: Mayer Resnick
American Physiological Society