ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2015) 38 P356 | DOI: 10.1530/endoabs.38.P356

Visceral fat drives 5[alpha]-reductase activity independent of BMI in women with polycystic ovarian syndrome

Punith Kempegowda1,2, Michael W O’Reilly1,2, Nicola J Crabtree1,2, Angela E Taylor1,2, Beverly A Hughes1,2, Jeremy W Tomlinson3 & Wiebke Arlt1,2

1Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, West Midlands, UK; 2Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, West Midlands, UK; 3Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, South East England, UK.

Context: Androgen excess, obesity and hyperinsulinaemia are the cardinal features of polycystic ovarian syndrome (PCOS). While several studies have addressed the relationship between androgen excess and hyperinsulinaemia, the link between androgen excess and fat distribution remains largely undefined. Recent work has highlighted the importance of adipose tissue as an organ of androgen activation. Here, we evaluated the relationship between visceral fat and androgen excess in women with PCOS.

Patients and methods: Seventeen women with PCOS were compared with 17 healthy volunteers matched for sex, age, and BMI. All subjects underwent BMI measurement and body composition assessment by dual-energy X-ray absorptiometry and assessment of their androgen status by measurement in serum and 24-h urine utilising mass spectrometry-based assays. A Pearson’s product-moment correlation coefficient was computed to assess the relationship between visceral adiposity and androgen generation.

Results: Women with PCOS, in comparison to healthy controls, had significantly higher visceral fat mass (944±593 g vs 406.1±378.9 g, P<0.01). Across the groups, there was a positive correlation between visceral fat mass and two urinary steroid metabolite ratios reflective of 5α-reductase activity, androstenedione/etiocholanolone (An/Et) (r=0.455, n=32, P=0.009), and 5α-tetrahydrocortisol/tetrahydrocortisol (5αTHF/THF) (r=0.443, n=32, P=0.011). 5α-reductase activity was significantly higher in PCOS compared to healthy controls (An/Et ratio 1.4±0.6 vs 1.1±0.3 and 5αTHF/THF 1.2±0.6 vs 0.8±0.3), and correlated significantly with visceral fat.

Conclusion: Our results lead us to hypothesise that visceral adiposity may drive androgen activation in PCOS by upregulation of 5α-reductase activity, which in turn results in further fat accumulation. Weight management is therefore likely to be a highly useful tool in ameliorating androgen excess in obese women with PCOS.

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