Insulin resistance, hypersecretion of LH, and a dual-defect hypothesis for the pathogenesis of polycystic ovary syndrome.

Abstract

Based on the available literature, we propose a "dual-defect" hypothesis of polycystic ovary syndrome. We suggest that in a significant subset of patients, this disorder may be caused by a conjunction of two independent genetic defects: one that produces elevated LH secretion and another that produces insulin resistance. Thus, polycystic ovary syndrome develops as a result of the synergistic action of increased LH levels and hyperinsulinemia on the ovary. This working hypothesis may serve as a useful guide for further studies of the pathogenesis of polycystic ovary syndrome.