J M Weiss1, S Polack, K Diedrich, O Ortmann. 1. Department of Gynecology and Obstetrics, Medical University Lübeck, Ratzeburger Allee 160, 23538 Luebeck, Germany.
Abstract
INTRODUCTION: Polycystic ovary syndrome (PCOS) is associated with insulin resistance and hyperinsulinemia, which might contribute to the hypersecretion of luteinizing hormone (LH). Hyperprolactinemia is another finding in a subgroup of patients with PCOS, whereas its relation to hyperinsulinemia is not fully understood yet. METHODS: In the present study we tested the hypothesis that insulin might affect LH or prolactin secretion of cultured female rat pituitary cells. To address the mechanisms by which insulin could act at the intracellular level we examined the GnRH- and TRH-induced Ca(2+) signals in single gonadotrophs and lactotrophs, because Ca(2+) is an important component of GnRH signal transduction that is closely related to exocytosis. RESULTS: Cells treated for 24 h with insulin (10(-9) M) showed an enhancement of basal and agonist-induced LH and prolactin secretion. Insulin did not affect GnRH- and TRH-induced Ca(2+) signals compared to controls. There were no differences neither in the frequency nor in the amplitude of the Ca signal. CONCLUSION: Our findings suggest that insulin might contribute to LH hypersecretion. Insulin might be partially responsible for hyperprolactinemia. Since insulin did not affect Ca signaling, other components of the GnRH signal transduction pathway might be involved in LH hypersecretion.
INTRODUCTION:Polycystic ovary syndrome (PCOS) is associated with insulin resistance and hyperinsulinemia, which might contribute to the hypersecretion of luteinizing hormone (LH). Hyperprolactinemia is another finding in a subgroup of patients with PCOS, whereas its relation to hyperinsulinemia is not fully understood yet. METHODS: In the present study we tested the hypothesis that insulin might affect LH or prolactin secretion of cultured female rat pituitary cells. To address the mechanisms by which insulin could act at the intracellular level we examined the GnRH- and TRH-induced Ca(2+) signals in single gonadotrophs and lactotrophs, because Ca(2+) is an important component of GnRH signal transduction that is closely related to exocytosis. RESULTS: Cells treated for 24 h with insulin (10(-9) M) showed an enhancement of basal and agonist-induced LH and prolactin secretion. Insulin did not affect GnRH- and TRH-induced Ca(2+) signals compared to controls. There were no differences neither in the frequency nor in the amplitude of the Ca signal. CONCLUSION: Our findings suggest that insulin might contribute to LH hypersecretion. Insulin might be partially responsible for hyperprolactinemia. Since insulin did not affect Ca signaling, other components of the GnRH signal transduction pathway might be involved in LH hypersecretion.