Evidence for visfatin as an independent predictor of endothelial dysfunction in polycystic ovary syndrome.

OBJECTIVE: Emerging evidence links adipocyte-secreted hormones, in particular adiponectin and visfatin, to cardiovascular pathology. Although adipocytokines dysregulation is common in polycystic ovary syndrome (PCOS) within the context of obesity and insulin resistance, their participation in the process of vascular injury remains elusive. DESIGN AND METHODS: This prospective, case-control study enrolled 102 young women (69 patients with PCOS and 33 eumenorrheic age-matched controls); serum adiponectin, resistin and visfatin, testosterone, SHBG, lipids, glucose, insulin, the homeostasis model assessment of insulin resistance (HOMA-IR) and high-sensitivity C-reactive protein (hs-CRP) were simultaneously measured in all participants. Body composition analysis was performed using dual X-ray absorptiometry. Endothelium impairment was assessed by carotid artery intimae-media thickness (CIMT) and brachial artery flow-mediated vasodilatation (FMD), respectively.
RESULTS: In PCOS, both univariate and multivariate analyses evidenced that circulating visfatin was significantly related to free testosterone (P = 0·024) and brachial artery FMD (P = 0·008; P < 0·01 in multivariate analyses). By every visfatin tertile, a stepwise decrease in FMD was observed in all and PCOS only (P = 0·036), not confounded by age, body mass index, total body fat mass, testosterone, SHBG or HOMA-IR. Multiple regression analysis retained visfatin and free testosterone as independent predictors of FMD, explaining about 20% of FMD variability. Adiponectin correlated with CIMT and hs-CRP, but the association was driven by age, body mass and body fat. No relationship between resistin and endothelial markers was found.
CONCLUSION: Visfatin may be a candidate to play a role in the pathogenesis of endothelial dysfunction in PCOS, independently of additional risk factors.