Gonadotropin secretory dynamics in polycystic ovary syndrome

Abstract

Whereas alterations in gonadotropin secretion have long been recognized in women with the polycystic ovary syndrome (PCOS), neither the mechanisms subserving these abnormalities nor the full ramifications of such altered secretion are completely understood. Within the past year several studies have examined fundamental aspects of gonadotropin secretion in PCOS, and the relation of such secretion to other hormonal systems. Increased serum LH concentrations in women with PCOS have again been shown to reflect both an increase in the number and amplitude of individual LH pulses and enhanced LH interpulse (basal) secretion. Perhaps paradoxically, short-term fasting in women with PCOS results in increased rather than decreased LH secretion. Whereas there is a strong positive relation between LH and inhibin B in women with PCOS, obesity negatively correlates with inhibin B in both normal and women with PCOS. Thus, the concentration of serum inhibin B in women with PCOS represents a balance between the positive and negative effects of LH and obesity, respectively. The LH secretory process itself in women with PCOS is disorderly, presumably reflecting abnormal regulation. Secretion of target hormones (eg, androstenedione) is also less orderly in women with PCOS. Moreover, the coupling of several hormone systems including LH–testosterone, LH–androstenedione and LH–leptin is disturbed in women with PCOS. The latter is consistent with the premise that both the feedforward (eg, LH stimulating testosterone secretion) and the feedback (eg, testosterone modulating the GnRH-LH secretory system) are deranged in PCOS.