Endocrine Abstracts (2017) 49 GP135 | DOI: 10.1530/endoabs.49.GP135

Brown adipose tissue thermogenesis in women with polycystic ovary syndrome

Soulmaz Shorakae1,2, Eveline Jona1, Barbora de Courten1,2, Gavin Lambert3,4, Elisabeth Lambert3, Sarah Phillips3, Iain Clarke5, Helena Teede1,2 & Belinda Henry6


1Monash Centre for Health Research and Implementation, Monash University, Melbourne, Australia; 2Diabetes and Vascular Medicine Unit, Monash Health, Melbourne, Australia; 3Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Australia; 4Department of Physiology, Monash University, Melbourne, Australia; 5Neuroscience Program, Monash Biomedicine Discovery Institute, Department of Physiology, Melbourne, Australia; 6Metabolic Disease and Obesity Program, Monash Biomedicine Discovery Institute, Department of Physiology, Melbourne, Australia.


Polycystic ovary syndrome (PCOS) is the most common endocrinopathy of reproductive age women and is characterized by reproductive, metabolic and psychological features exacerbated by weight gain. Weight management in PCOS is challenged by propensity to weight gain and lack of sustainable dietary interventions. Body weight is regulated by calorie intake and the rate of energy expenditure. Metabolically active brown adipose tissue (BAT), contributing to energy dissipation, has been described in humans. The thermogenic activity of BAT is controlled by the sympathetic nervous system (SNS). Sex hormones also play role in modulating BAT. Human studies confirm association of supraclavicular skin temperature, where most human BAT is located, with BAT activity. This observational study aimed to explore BAT thermogenesis and its associations, for the first time, in PCOS. Cutaneous wireless temperature probes (2 cm diameter, 0.5 depths) were taped to supraclavicular (BAT) and upper arm (muscle) regions of 49 premenopausal women with PCOS, over 96 hours, (mean age: 29.85±5.93, mean BMI: 29.02±5.43), recruited from community. Multiunit muscle SNS activity (by microneurography) and plasma noradrenaline levels were measured as markers of SNS activity. Fasting lipids, serum androgens, markers of insulin resistance and inflammation were measured. Recorded temperature data from both regions were available in 41 participants. Supraclavicular temperature was significantly higher than arm temperature (33.87±0.65 vs 32.23±0.85, P < 0.0001). Supraclavicular temperature correlated with testosterone (r=−0.410, P=0.011), noradrenaline (r=−0.488, P=0.005) and triglycerides (r=−0.393, P=0.015) which remained significant after adjustment for BMI. Arm temperature did not correlate with testosterone, noradrenaline and triglycerides. This is the first study of BAT thermogenesis in PCOS using cutaneous temperature probes. The negative correlation of BAT temperature with noradrenaline levels could implicate a maladaptive thermogenic response to chronic SNS activation in PCOS. Chronic sympathoexcitation and hyperandrogenism play potential roles in modulation of BAT thermogenesis in PCOS.

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