Evidence for insulin suppression of baseline luteinizing hormone in women with polycystic ovarian syndrome and normal women.

Abstract

In women with polycystic ovarian syndrome (PCOS), the relationship of insulin to LH secretion and responses to GnRH remains unresolved. A rigorous analytical examination of this relationship has not been performed. Our objective was to determine the relationship of basal LH secretion and responses to GnRH, insulin, and other endocrine variables in normal and PCOS women. In PCOS and normal women, mean composite 12-h LH secretion was analyzed for correlating factors. LH responses to varying doses of GnRH during a fixed rate of insulin infusion and LH responses to a fixed dose of GnRH during varying doses of insulin infusion were analyzed for contributing factors. Eighteen PCOS and 21 normal women underwent studies of frequent blood sampling and GnRH stimulation before and during insulin infusion at the General Clinical Research Center, University of California, San Diego. Group mean composite 12-h LH levels were assessed with respect to other endocrine variables. In addition, LH responses to GnRH with or without insulin infusion were assessed. In normal women, insulin negatively predicted mean LH. In PCOS, the combined effect of body mass index (negative) and testosterone (positive) predicted LH. The best predictor of LH was body mass index and insulin combined. Basal LH and LH responses to GnRH were unaltered by insulin infusion in normal women. These measures were reduced during insulin infusion in PCOS women. In PCOS, insulin infusion suppresses pituitary response to GnRH. In normal women, insulin negatively correlates with mean LH and suppresses GnRH response at a high infusion rate.