Related Experiment Video
Updated: Jun 5, 2026
A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
Published on: October 2, 2018
Hyperandrogenism in women with polycystic ovary syndrome persists after menopause
Marios C Markopoulos1, Demetrios Rizos, George Valsamakis
1Second Department of Obstetrics and Gynecology, Athens University Medical School, Aretaieion Hospital, Athens 11528, Greece.
Context:
Ovarian and adrenal hyperandrogenism characterize premenopausal women with polycystic ovary syndrome (PCOS). Androgens decline with age in healthy and PCOS women.
Objective:
The objective of the study was to investigate hyperandrogenism in PCOS after menopause.
Design:
This was a case-control, cross-sectional study.
Setting:
The study was conducted at a university hospital endocrinology unit.
Patients:
Twenty postmenopausal women with PCOS and 20 age- and body mass index-matched controls participated in the study.
Interventions:
Serum cortisol, 17-hydroxyprogesterone (17-OHP), Δ(4)-androstenedione (Δ(4)A), dehydroepiandrosterone sulfate (DHEAS), total testosterone (T), and free androgen index (FAI) levels were measured at baseline, after ACTH stimulation, and after 3-d dexamethasone suppression. The ACTH and cortisol levels were measured during the CRH test.
Main Outcome Measures:
Androgen profile at baseline, after ACTH stimulation, and 3-d dexamethasone suppression tests were the main outcome measures.
Results:
Postmenopausal PCOS women had higher 17-OHP, Δ(4)A, DHEAS, total T, FAI (P < 0.05) and lower SHBG (P < 0.05) baseline levels than control women. ACTH and cortisol responses during the CRH test were similar in the two groups. After ACTH stimulation, Δ(4)A, DHEAS, and total T levels were equally increased in both groups. After dexamethasone suppression, LH levels did not change in either group; 17-OHP-, Δ(4)A-, and FAI-suppressed levels remained higher in PCOS than in control women (P < 0.05), whereas total T and DHEAS levels were suppressed to similar values in both groups.
Conclusions:
In postmenopausal PCOS women, ACTH and cortisol responses to CRH are normal. Androgen levels at baseline are higher in PCOS than control women and remain increased after ACTH stimulation. The dexamethasone suppression results in postmenopausal PCOS women suggest that DHEAS and total T are partially of adrenal origin. Although the ovarian contribution was not fully assessed, increased Δ(4)A production suggests that the ovary also contributes to hyperandrogenism in postmenopausal PCOS women. In conclusion, postmenopausal PCOS women are exposed to higher adrenal and ovarian androgen levels than non-PCOS women.
Related Concept Videos
01:28Menopause
01:30Hormonal Control of the Ovarian Cycle
Before puberty, the hypothalamus releases GnRH in a low frequency, low amplitude pulsatile manner. This along with the immature hypothalamic-pituitary-gonadal axis activity, results in low estrogen levels and the absence of a fully functional ovarian cycle. At puberty, GnRH secretion increases in both frequency and...
02:07Oogenesis
01:22Oogenesis
Each primary oocyte is surrounded by a layer of pre-granulosa cells, forming what is known...
01:24Disorders of the Female Reproductive System
01:22Hormonal Regulation of the Menstrual Cycle
At puberty, GnRH begins a pulsatile release pattern, which triggers the anterior pituitary gland to secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The frequency and amplitude of GnRH pulses vary across the menstrual cycle, with faster pulses favoring LH release and slower pulses favoring FSH release.