The role of Visfatin in atherosclerotic peripheral arterial obstructive disease Matthaios G. Pitoulias a,d , Lemonia Skoura b , Apostolos G. Pitoulias c , Dimitris Chatzidimitriou b , Apostolia Margariti b , Minas Arsenakis d , Georgios A. Pitoulias c,⇑ a Centre for Bimolecular Science, Faculty of Science, University of Nottingham, UK b Department of Microbiology, School of Medicine, Aristotle University of Thessaloniki, Greece c 2nd Department of Surgery, Division of Vascular Surgery, Aristotle University of Thessaloniki, Greece d Laboratory of General Microbiology, School of Biology, Aristotle University, Thessaloniki, Greece article info Article history: Received 27 November 2016 Received in revised form 19 December 2016 Accepted 25 December 2016 Keywords: Visfatin Adipokine Atherosclerosisl Peripheral arterial obstructive disease abstract Visfatin is an adipokine molecule acting as an essential coenzyme in multiple cellular redox reactions. The increased serum levels of Visfatin have been correlated with metabolic syndrome and endothelial homeostasis. In this study we investigate the possible relationship of Visfatin serum levels with the severity and location of atherosclerotic peripheral arterial occlusive disease (PAOD). Study protocol included 45 consecutive PAOD and 20 Control patients with age >55 years old. Definition of PAOD was based in Rutherord’s classification (RC). End-stage PAOD patients (RC-V & -VI) were excluded from study. Data were collected prospectively and included age, gender, atherosclerotic risk factors and the body mass index (BMI). In PAOD patients recorded the PAOD’s clinical stage and the presence of carotid stenosis >50%. PAOD patients divided in two subgroups, those with mild (RC-I & -II) and moderate disease (RC-III & -IV). In all serum samples Visfatin was measured, blindly, twice by anosoenzymatic technique. Statistical analysis was performed by non-parametric Mann-Whitney U test, Pearson’s chi-square, One Way Anova and Kruskall-Wallis tests, as appropriate. The mean Visfatin value in PAOD and Control groups were 38.5 ± 16.0 and 13.9 ± 3.8 ng/ml respectively (p < 0.0005). In-PAOD subgroup of patients the visfatin values were not affected by demographics, BMI and atherosclerotic risk factors (p > 0.05). Univariate analysis showed that severity of PAOD (mild vs sev- ere), presence of carotid stenosis >50% and multilevel disease significantly affected outcomes (p = 0.018, p = 0.010 and p = 0.006 respectively). In multivariate regression analysis severity of PAOD was the solely factor with strong correlation with high visfatin values (p = 0.001). High Visfatin levels seem to be strongly correlated with the presence and severity of PAOD. Further and in depth investigation is needed to define the possible role of Visfatin in atherosclerosis and it’s value as a potential prognostic biomarker of PAOD. Ó 2017 Elsevier Ltd. All rights reserved. 1. Introduction Visfatin is an adipokine molecule which displays intrinsic enzy- matic activity as a nicotinamide phosphoribosyltransferase (Nampt) [1]. Visfatin/Nampt, in mammals, is involved in synthesis of nicotinamide adenine nucleotide (NAD+) which act as an essen- tial coenzyme in multiple cellular redox reactions [2]. Obesity and type 2 diabetes represent two well-known independent risk factors of inflammation related to atherosclerotic arterial disease. Although, a positive role of Visfatin in these two factors has been proposed, the ongoing investigation shows that this potential role still remains controversial [3]. Additionally, in humans the increased serum levels of Visfatin have been correlated with meta- bolic syndrome and carotid atherosclerosis [4]. A potentially indi- rect role of visfatin in cardiovascular diseases has been supposed, through the metabolic syndrome and inflammation. Furthermore, direct actions with smooth muscle cells proliferation and angio- genesis, with increased levels and activity of matrix metallopro- teinases (MMP 2 and 9) as well as with promotion of cell adhesion molecules like the ICAM-1, VCAM-1 and E-selectin has also been proposed [2,5]. All these actions, especially in combina- http://dx.doi.org/10.1016/j.cyto.2016.12.027 1043-4666/Ó 2017 Elsevier Ltd. All rights reserved. ⇑ Corresponding author at: 2nd Department of Surgery, Division of Vascular Surgery, Aristotle University of Thessaloniki, «G. Gennimatas» Hospital, 41 Ethnikis Aminis str, Thessaloniki 54635, Greece. E-mail addresses: pitoulias@yahoo.com, pitulias@med.auth.gr (G.A. Pitoulias). Cytokine 91 (2017) 140–144 Contents lists available at ScienceDirect Cytokine journal homepage: www.journals.elsevier.com/cytokine