Insulin and the Polycystic Ovary Syndrome

Abstract

The cardinal clinical manifestations of the polycystic ovary syndrome are hirsutism and anovulation, oligomenorrhea, or amenorrhea. About half the women with this syndrome are obese, and some have diabetes mellitus. Underlying these clinical abnormalities is an array of biochemical abnormalities that have defied simple explanation. Among them, the most important are increased serum concentrations of total and free testosterone, decreased serum sex hormone–binding globulin concentrations, increased serum luteinizing hormone concentrations, and hyperinsulinemia. Not all affected women have all these biochemical abnormalities, but in the aggregate, these findings, along with the clinical abnormalities, are characteristic of the syndrome.¹ Anatomically, most of . . .