Abstract
Sympathetic nervous system (SNS) activity is increased in polycystic ovary syndrome (PCOS). Moxonidine is a centrally acting sympatholytic drug with known beneficial effects on hypertension, insulin sensitivity, dyslipidemia and inflammation. In this double-blind placebo controlled randomized clinical trial we examined the effect of moxonidine on modulating sympathetic activity and downstream metabolic abnormalities in 48 pre-menopausal women with PCOS (Rotterdam diagnostic criteria), recruited from the community (January 2013–August 2015). Participants received moxonidine (0.2 mg daily initially, up titrated to 0.4 mg daily in 2 weeks) (n = 23) or placebo (n = 25) for 12 weeks. Multiunit muscle sympathetic activity (by microneurography) and plasma noradrenaline levels were measured (primary outcomes). Fasting lipids, insulin resistance, serum androgens, and inflammatory markers were measured as secondary outcomes. Forty three women completed the trial (19 moxonidine, 24 placebo). Mean change in burst frequency (−3 ± 7 vs. −3 ± 8 per minute) and burst incidence (−3 ± 10 vs. −4 ± 12 per 100 heartbeat) did not differ significantly between moxonidine and placebo groups. Women on moxonidine had a significant reduction in hs-CRP compared to placebo group (−0.92 ± 2.3 vs. −0.04 ± 1.5) which did not persist post Bonferroni correction. There was a significant association between markers of insulin resistance at baseline and reduction in sympathetic activity with moxonidine. Moxonidine was not effective in modulating sympathetic activity in PCOS. Anti-inflammatory effects of moxonidine and a relationship between insulin resistance and sympathetic response to moxonidine are suggested which need to be further explored.Clinical Trial Registration Number: (NCT01504321)
Highlights
Polycystic ovary syndrome (PCOS) is a common endocrinopathy of reproductive age women, affecting 12–18%, with hyperinsulinemia and hyperandrogenism being the key hormonal features underpinning the pathophysiology of the disease (Dunaif, 1997; March et al, 2010; Teede et al, 2011)
Increasing evidence arising from animal and human studies favors the role of increased sympathetic nervous system (SNS) activity in the pathophysiology of PCOS (Lara et al, 1993, 2002; Greiner et al, 2005; StenerVictorin et al, 2005; Yildirir et al, 2006; Sverrisdottir et al, 2008)
We demonstrated that mean change in burst frequency significantly correlated with post OGTT glucose and fasting insulin and mean change in burst incidence significantly correlated with fasting insulin and HOMA-insulin resistance (IR) at baseline
Summary
Polycystic ovary syndrome (PCOS) is a common endocrinopathy of reproductive age women, affecting 12–18%, with hyperinsulinemia and hyperandrogenism being the key hormonal features underpinning the pathophysiology of the disease (Dunaif, 1997; March et al, 2010; Teede et al, 2011). Additional to reproductive features, PCOS is associated with a range of metabolic abnormalities including insulin resistance (IR) and impaired glucose tolerance (IGT), gestational diabetes, type 2 diabetes, dyslipidemia, obstructive sleep apnoea (OSA) and an increased risk of cardiovascular disease (Teede et al, 2011; Shorakae et al, 2014; Hart and Doherty, 2015). This increased risk of cardiometabolic abnormalities in PCOS, at least in part, is attributed to the interrelated effects of hyperandrogenism, IR, sympathetic nervous system (SNS) dysfunction and chronic low grade inflammation (Shorakae et al, 2015). Electro-acupuncture, physical exercise and renal denervation have effectively modulated SNS in women with PCOS and generated beneficial effects on ovulation, hyperandrogenism and oligomenorrhea (Stener-Victorin et al, 2000b, 2009; Jedel et al, 2011; Schlaich et al, 2011; Johansson et al, 2013)
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