THE INFLUENCE OF LUTEINIZING-HORMONE AND INSULIN ON SEX STEROIDS AND SEX HORMONE-BINDING GLOBULIN IN THE POLYCYSTIC OVARIAN SYNDROME

Objective: To examine the relationship between hyperinsulinemia, sex h ormone-binding globulin (SHBG), and body mass index (BMI) on LH-induce d hyperandrogenemia in patients with polycystic ovarian syndrome (PCOS ). Design: Insulin responses during an oral glucose tolerance test (OG TT) were assessed in 25 consecutive women with PCOS and 20 control wom en matched for BMI. Insulin responses and sensitivity (S(I)) were also determined using a frequently sampled intravenous glucose tolerance t est (IVGTT). Setting: The clinical research center at a university med ical center. Main Outcome Measures: Serum LH, S(I) and basal, peak, an d area under the curve (AUC-insulin responses) were determined and cor related with SHBG, androstenedione (A), T, and free T concentrations. Results: Compared with controls, the AUC-insulin response during OGTT was greater in PCOS, with an average increase of 44%. During IVGTT, AU C-insulin response was also significantly higher in PCOS versus contro ls, with an average increase of 53%. In addition, S(I) was reduced in PCOS versus controls with an average decrease of 53%. The average diff erences in oral- and intravenous-glucose-induced hyperinsulinemia and in insulin sensitivity between PCOS and controls were relatively const ant across the entire physiological range of BMI. In PCOS, baseline LH showed strong positive correlations with baseline A and T. However, t here were no significant correlations between either basal, peak, or A UC-insulin response during OGTT and IVGTT with basal T or A concentrat ions or between insulin and androgen levels measured at 30-minute inte rvals throughout the OGTT. However, basal, peak, and AUC-insulin respo nses during OGTT were strongly correlated with fasting SHBG binding ca pacity. Conclusions: These data are consistent with the hypothesis tha t hyperinsulinemia in PCOS influences the biologically active componen t of T by lowering SHBG concentrations while having little apparent im pact on LH-induced secretion of androgens in vivo.