Sympathetic activation and endothelial dysfunction in polycystic ovary syndrome are not explained by either obesity or insulin resistance

摘要: SummaryObjective Polycystic ovary syndrome (PCOS) is a common endocrine condition underpinned by insulin resistance and associated with increased risk of obesity, type 2 diabetes adverse cardiovascular profile. Previous data suggest autonomic imbalance [elevated sympathetic nervous system (SNS) activity decreased heart rate variability (HRV)] as well endothelial dysfunction in PCOS. However, it not clear whether these abnormalities are driven obesity metabolic disturbance or they independently related to PCOS. Participants methods We examined multiunit single-unit muscle SNS (by microneurography), HRV (time frequency domain analysis) function [ischaemic reactive hyperaemia index (RHI) using the EndoPAT device] 19 overweight/obese women PCOS (BMI: 31·3 ± 1·5 kg/m2, age: 31·3 ± 1·6 years) compared them 21 control 33·0 ± 1·4 kg/m2, 28·2 ± 1·6 years) presenting similar profile (fasting total, HDL LDL cholesterol, glucose, triglycerides, sensitivity blood pressure). Results Women had elevated (41 ± 2 vs 33 ± 3 bursts per 100 heartbeats, P < 0·05). Single-unit analysis showed that vasoconstrictor neurons were characterized firing probability incidence multiple spikes (P < 0·01 for all parameters). Women also impaired (RHI: 1·77 ± 0·14 2·18 ± 0·14, did differ between groups. Conclusion Women have drive independent disturbances. Sympathetic activation may confer greater