Increased luteinizing hormone secretion in women with polycystic ovary syndrome is unaltered by prolonged insulin infusion.

In PCOS women with insulin resistance, hyperinsulinemia may contribute to inappropriate gonadotropin secretion. To determine whether insulin influences gonadotropin release in PCOS, pulsatile LH secretion and gonadotropin responses to GnRH were evaluated before (phase 1) and during (phase 2) insulin infusion. In phase 1, 11 PCOS and 9 normal women on separate days underwent 1) frequent blood sampling (q 10 min) for 12 h and 2) gonadotropin stimulation by successive doses of GnRH, 2 microg, 10 microg, and 20 microg, administered i.v. at 4 h intervals over a continuous 12 h. In phase 2, studies were repeated 2 h after initiation of a 12-h hyperinsulinemic-euglycemic clamp (80 mU/m(2).min). Administration of insulin to both groups failed to alter mean serum gonadotropin concentrations, LH pulse frequency, or LH pulse amplitude. Moreover, gonadotropin responses to GnRH were unchanged by insulin infusion. In PCOS and normal women, a significant reduction of serum androstenedione was associated with insulin administration, whereas no differences were noted for the remaining androgens and estrogens measured. These findings demonstrated that in PCOS women, LH secretion and gonadotropin responses to GnRH were not influenced by insulin administration. Insulin infusion had little effect on steroid hormone production with the possible exception of androstenedione. These results suggest that inappropriate LH secretion in PCOS is not a direct consequence of insulin resistance and compensatory hyperinsulinemia.