The Joint Annual Scientific Meetings of the Endocrine Society of Australia and the Society for Reproductive Biology 2018

Experimental polycystic ovary syndrome (PCOS) traits can be ameliorated by dietary intervention (#130)

Valentina Rodriguez Paris 1 , Samantha M Solon-Biet 2 , Melissa C Edwards 1 3 , Madeleine J Cox 1 , William L Ledger 1 , Robert B Gilchrist 1 , Stephen J Simpson 2 , David J Handelsman 3 , Kirsty A Walters 1 3
  1. School of Women's & Children's Health, University of New South Wales, Sydney, NSW 2052, Australia
  2. Charles Perkins Centre, University of Sydney , Sydney, NSW 2006, Australia
  3. ANZAC Research Institute, University of Sydney , Sydney, NSW 2139, Australia

Polycystic ovary syndrome (PCOS) is a complex disorder characterized by reproductive, endocrine and metabolic abnormalities; however, its aetiology is unknown and current medical management relies solely on symptomatic treatment. Hyperandrogenism is a defining characteristic of PCOS, and diet is inherently associated since obesity is present in 40-80% of PCOS women. Yet, the optimal diet for PCOS treatment remains undefined. Therefore, to determine the impact of dietary macronutrient balance on the development of PCOS, we provided our experimental mouse model of dihydrotestosterone (DHT)-induced PCOS and control mice with ad libitum access to one of 10 diets varying in protein (P), carbohydrate (C) and fat (F) content. PCOS mice exhibit complete estrous acyclicity, but despite the presence of hyperandrogenism, cyclicity was restored in PCOS mice on a relatively balanced diet of P:C (ratio of 1:1.5; p<0.05), with fat having a negligible effect. Ovaries collected from PCOS mice with diet restored cyclicity exhibited corpora lutea, confirming the occurrence of ovulation. Interestingly, PCOS mice with restored cyclicity were not the leanest PCOS females observed, displaying a higher average body weight (24.4g +/- 0.2) compared to controls (21.7g +/- 0.2, p<0.001). In PCOS mice, obesity was minimised on a high P diet (P:C ratio of 2:1), with a reduction of adipocyte size correlating with a decrease in C intake (p<0.05). As a measure of energy expenditure, uncoupling protein 1 (UCP1) expressed in brown adipose tissue was 42% higher (p<0.05) in PCOS mice compared to controls, independent of diet. PCOS mice on diets with restored cyclicity had equivalent UCP1 levels to the peak UCP1 levels of control females. These findings demonstrate that PCOS traits can be ameliorated through dietary interventions to restore reproductive and metabolic abnormalities to control levels, although it appears that these hallmark PCOS traits are differentially affected by diet.