Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2004) 8 P78

SFE2004 Poster Presentations Reproduction (8 abstracts)

Androgens inhibit atresia and retard early development of ovarian follicles: a model for PCOS?

AI Qureshi 1 , G Bano 2 , S Whitehead 1 , SS Nussey 2 & HD Mason 3


1Department of Basic Medical Sciences, St George's Hospital Medical School, London, SW17 ORE, UK; 2Department of Cellular & Molecular Medicine, St George's Hospital Medical School, London, SW17 ORE, UK; 3Departments of Clinical Developmental Sciences and Basic Medical Sciences, St George's Hospital Medical School, London, SW17 0RE, UK.


Background

PCOS is the commonest endocrinopathy in women. PCO are typified by increased ovarian follicles. The aetiology is unknown, but may be due either to enhanced follicular growth, reduced atresia, or both. Hyperandrogenism is almost universal either clinically or biochemically and in primates and sheep androgen excess in-utero produces ovaries phenotypically identical to those in PCOS. There have been no analyses of the effects of androgens on early follicle growth and atresia.

Aims

To determine the effects of androgens on lamb ovarian follicular growth and atresia.

Methods

Fragments of lamb ovarian cortex were cultured on the chorioallantoic membrane of 5-6 day old fertilised chick eggs (Qureshi et al, 2003) for 5 days. Four treatment groups were established: testosterone (10-7M), FSH (0.05 iu/ml), FSH and testosterone and control, added in 10 microlitres of medium to implanted tissue. An experiment using tritiated androgen revealed stable distribution in the various egg compartments. After 5 days, the retrieved tissue was fixed, sectioned and stained. Follicles were counted, staged (Nikon ACT version 2 software) and compared with unimplanted baseline tissue and implanted untreated control tissue.

Results

The percentage of follicles in each category for each treatment was as follows. Results are in the order primordial, transitional, primary, secondary and atretic in each case. Baseline (n=352) 66.48%, 23.01%, 9.38%, 1.14%, 8.31%: Control (n=328) 59.45%, 25.30%, 10.98%, 4.27%, 18.91%: Testosterone (n=801) 66.04%, 14.23%, 18.48%, 1.25%, 8.34%: FSH (n=339) 53.98%, 24.78%, 17.40%, 3.83%, 10.51%: Testosterone and FSH (n=293) 55.29%, 22.18%, 17.06%, 5.46%, 13.76%.

In summary, testosterone inhibited recruitment of resting follicles, transition from primary to secondary and, like FSH, reduced rates of atresia.

Discussion

These results provide a possible explanation for the phenotypical changes seen in PCO. Given the reported increase in primordial follicle density in PCO (Webber et al, 2003) these effects of androgens may occur in-utero.

Volume 8

195th Meeting of the Society for Endocrinology joint with Diabetes UK and the Growth Factor Group

Society for Endocrinology 

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