Opioidergic regulation of LH pulsatility in women with polycystic ovary syndrome
Berga, S.L.; Yen, S.S.
Clinical Endocrinology 30(2): 177-184
1989
ISSN/ISBN: 0300-0664 PMID: 2532984 DOI: 10.1111/j.1365-2265.1989.tb03739.xDocument Number: 369439
To determine whether the disordered patterns of luteinizing hormone (LH) pulsatility and impaired opioidergic regulation of gonadotropin- releasing hormone (GnRH)-LH observed in women with polycystic ovarian syndrome reflect an inherent hypothalamic abnormality or a functional state related to the acyclycity of sex steroids, medroxyprogesterone acetate was administered to 6 women with this syndrome. It was hypothesized that if the apparent lack in women with polycystic ovarian syndrome of opiodergic regulation of GnRH-LH release was in fact secondary to an inherent hypothalamic defect, then the administration of this progestogen would fail to produce opiodergic regulation of GnRH-LH. Medroxyprogesterone acetate was given orally to the 6 study subjects over a 10-day period in an incremental dosage to mimic the luteal phase. LH pulsatility and follicle-stimulating hormone (FSH) levels were measured at 10 minute intervals during the 8 hours before and after treatment and infusions of saline or naloxone were given. All 6 subjects showed significant changes in LH pulsatile activities after steroid administration, specifically a slowing of LH pulse frequency and an increase in pulse amplitude and duration. Naloxone infusion reversed these progestogen-associated changes. There were no changes in mean LH, mean FSH, androgen, or estrogen levels, however, suggesting that a luteal phase LH pulse pattern was produced. Since naloxone reversed the changes in LH pulsatility induced by medroxyprogesterone acetate, it can be concluded that these responses involved the induction of central opiodergic activity secondary to ovarian acyclycity and progesterone deficiency, not a primary hypothalamic defect.