Mohamed F M Mitwally1, Robert F Casper. 1. Department of Obstetrics and Gynecology, Samuel Lunenfeld Research Institute and Mount Sinai Hospital, University of Toronto, Ontario, Canada.
Abstract
PURPOSE: To investigate hCG and insulin-stimulated progesterone (P) production by human granulosa-lutein cells (hGLC) in vitro. METHODS: hGLCs were isolated from patients undergoing IVF-ET cycles in whichGnRH agonist or GnRH antagonist was used to prevent a midcycle gonadotropin surge. The cells were cultured for 3 days, and then treated with hCG 0.5, 1, and 10 IU/I, and insulin 0.01, 0.1, and 1 microM in serum free conditions. In vitro P production was measured by enzyme immunoassay. RESULTS:hCG stimulated P production by hGLCs from cycles in which GnRH antagonist was used, but a blunted response was seen in GnRH-agonist treated cycles. Insulin-stimulated P production was similar in cells from cycles in which GnRH-agonist or GnRH-antagonist treatment was used. CONCLUSIONS: Because insulin and hCG may share common pathways beyond the level of receptor activation, we hypothesize that GnRH agonist, but not GnRH antagonist, may affect the expression and/or activation of LH receptors in the hGLCs.
RCT Entities:
PURPOSE: To investigate hCG and insulin-stimulated progesterone (P) production by human granulosa-lutein cells (hGLC) in vitro. METHODS: hGLCs were isolated from patients undergoing IVF-ET cycles in which GnRH agonist or GnRH antagonist was used to prevent a midcycle gonadotropin surge. The cells were cultured for 3 days, and then treated with hCG 0.5, 1, and 10 IU/I, and insulin 0.01, 0.1, and 1 microM in serum free conditions. In vitro P production was measured by enzyme immunoassay. RESULTS:hCG stimulated P production by hGLCs from cycles in which GnRH antagonist was used, but a blunted response was seen in GnRH-agonist treated cycles. Insulin-stimulated P production was similar in cells from cycles in which GnRH-agonist or GnRH-antagonist treatment was used. CONCLUSIONS: Because insulin and hCG may share common pathways beyond the level of receptor activation, we hypothesize that GnRH agonist, but not GnRH antagonist, may affect the expression and/or activation of LH receptors in the hGLCs.
Authors: J M Weiss; K Oltmanns; E M Gürke; S Polack; F Eick; R Felberbaum; K Diedrich; O Ortmann Journal: Eur J Endocrinol Date: 2001-06 Impact factor: 6.664