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Origin of serum progestins in polycystic ovarian disease
Abstract:
The glandular origin of excess circulating steroid hormones in women with polycystic ovarian disease has been difficult to establish with previously described perturbation techniques. Recently it was demonstrated that daily administration of a potent gonadotropin-releasing hormone agonist achieves complete and reversible suppression of ovarian steroid secretion. To examine the source of C-21 steroid hormones, circulating levels were measured before and after administration of the same agonist in polycystic ovarian disease subjects and normal control subjects. Serum levels of these hormones were also determined after administration of dexamethasone and adrenocorticotropic hormone (ACTH) as well as bilateral oophorectomy. Subjects with polycystic ovarian disease exhibited significant elevations of serum pregnenolone, 17OH -pregnenolone, and 17OH -progesterone by comparison with normal control subjects. The glandular origins of the excess levels of pregnenolone and 17OH -pregnenolone were more difficult to determine and appear to be different from that of 17OH -progesterone.
Insights
This study investigated the source of excess steroid hormones in polycystic ovarian disease (PCOD). Gonadotropin-releasing hormone agonist treatment helped identify that while 17OH-progesterone
Area of Science:
- Endocrinology
- Reproductive Biology
- Steroidogenesis
Background:
- Polycystic ovarian disease (PCOD) is associated with elevated circulating steroid hormones.
- The specific glandular origin of these excess steroids in PCOD has been challenging to determine.
- Previous perturbation techniques have had limitations in pinpointing steroid hormone sources.
Purpose of the Study:
- To investigate the glandular origin of excess C-21 steroid hormones in women with PCOD.
- To utilize a gonadotropin-releasing hormone agonist to suppress ovarian steroid secretion and assess hormonal sources.
- To compare steroid hormone levels in PCOD subjects and normal controls under various hormonal challenges.
Main Methods:
- Administration of a potent gonadotropin-releasing hormone agonist to suppress ovarian steroid secretion.
- Measurement of serum steroid hormone levels (pregnenolone, 17OH-pregnenolone, 17OH-progesterone) before and after agonist treatment.
- Assessment of hormone levels following administration of dexamethasone, adrenocorticotropic hormone (ACTH), and after bilateral oophorectomy.
Main Results:
- Women with PCOD showed significantly elevated serum levels of pregnenolone, 17OH-pregnenolone, and 17OH-progesterone compared to controls.
- The glandular origins of elevated pregnenolone and 17OH-pregnenolone were less definitively determined.
- The source of excess 17OH-progesterone appeared distinct from that of pregnenolone and 17OH-pregnenolone.
Conclusions:
- The study provides insights into the complex steroidogenesis in PCOD.
- Different glandular origins contribute to the elevated steroid hormone profiles observed in PCOD.
- Further research is needed to fully elucidate the specific sources of pregnenolone and 17OH-pregnenolone in PCOD.