Abstract
This thesis identifies and addresses important knowledge gaps in our understanding of PCOS pathophysiology, also generates new insights into the mechanisms underlying increased cardiometabolic risks in PCOS. I examined the role of sympathetic dysfunction and chronic low grade inflammation in the pathophysiology of PCOS. My findings suggest a close association of sympathetic activity with chronic low-grade inflammation and with development of insulin resistance, hyperandrogenism and potentially the subsequent metabolic abnormalities in PCOS. I report moxonidine is not effective in modulating sympathetic activity in PCOS however may exert anti-inflammatory effects. This will inform future clinical trials in amelioration of PCOS features.
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