Invited editorial Adipokine profile as a novel screening method for cardiometabolic disease: Help or hindrance? Ivana Veljic ´ 1 , Marija Polovina 1,2 , Jelena P Seferovic ´ 2,3 and Petar M Seferovic ´ 1,2 Adipose tissue acts as a dynamic endocrine organ pro- ducing adipokines, a family of peptides with heteroge- neous metabolic activities. 1 Several adipokines (e.g. tumour necrosis factor-a (TNF-a), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), adipsin, chemerin, nerve growth factor (NGF), soluble serum amyloid A1 (SAA1), resistin, migration inhibi- tory factor (MIF), plasminogen activator inhibitor-1 (PAI-1) and hepatic growth factor (HGF)) have been found to exert adverse metabolic and vascular effects through their proinflammatory and prothrombotic effects. 1 Of note, increased levels of resistin and related adipokines have been shown to independently increase the risk of vascular events by 44% in healthy individ- uals. 2 Conversely, leptin, adiponectin, apelin and visfa- tin have been distinguished by their anti-inflammatory and insulin-sensitizing properties. 1,3,4 Higher adiponec- tin levels, acting by down-regulation of proinflamma- tory mediators and by improving endothelial function, 5,6 have been associated with improvement of some metabolic syndrome characteristics 7 and with less severe cardiac ischaemia and reperfusion injury follow- ing an acute myocardial infarction. 8 There is evidence suggesting that adverse metabolic and cardiovascular effects result from complex changes in the composition and metabolism of adipose tissue (i.e. adipose tissue dysfunction (ATD)). ATD is characterized by a sig- nificant imbalance in adipokine profile, with a predom- inance of proinflammatory and prothrombotic adipokines. 9 This is frequently seen in obesity, but it can also occur in normal-weight individuals and is strongly related to visceral adiposity, 10 a hallmark of the metabolic syndrome. 11 However, the character- istics of ATD and its association with the metabolic syndrome are not fully elucidated. Therefore, clarifying these issues may be relevant for the guidance of pharmacological and lifestyle interventions. In the current issue of the European Journal of Preventive Cardiology, Schrover and colleagues explore the relationship between 11 adipokines considered to reflect ATD, regional body fat distribution and the like- lihood of the metabolic syndrome in a cross-sectional study including 1215 patients with various vascular diseases. The association between adipokines and the metabolic syndrome was assessed for individual adipo- kines and for an ‘adipokine profile’, which was con- structed by summation of equally weighted quartiles of all analysed adipokine levels. Adiposity parameters included body mass index (BMI), waist circumference, subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT), as assessed by echo sonography. 12 The results of the present study showed that higher BMI, waist circumference and VAT correlated with increased levels of NGF, HGF, MIF, leptin and adip- sin, and the strongest positive relation was found between BMI, adipsin and leptin. Conversely, an inverse relation was seen between adiposity parameters and chemerin, PAI-1, resistin, SAA1 and adiponectin. The strongest negative relation was found between BMI and SAA1 and between VAT and adiponectin. Importantly, there was no significant relationship between SAT and adipokine levels. Following adjustment for potential confounders, HGF and leptin were found to increase the likelihood of the metabolic syndrome by 21% and 26%, respect- ively. On the other hand, adiponectin and resistin appeared to have a protective role, as they both decreased the likelihood of the metabolic syndrome, by 27% and 15%, respectively. Finally, in the multi- variable analysis, each point higher sum of adipokines, expressed as the adipokine profile, increased the 1 Department of Cardiology, Clinical Centre of Serbia, Belgrade, Serbia 2 School of Medicine, Belgrade University, Serbia 3 Department of Endocrinology, Clinical Centre of Serbia, Belgrade, Serbia Corresponding author: Petar M Seferovic ´, School of Medicine, Belgrade University, 8 Dr Subotic ´a, 11000 Belgrade, Serbia. Email: seferovic.petar@gmail.com European Journal of Preventive Cardiology 2018, Vol. 25(14) 1543–1547 ! The European Society of Cardiology 2018 Article reuse guidelines: sagepub.com/journals-permissions DOI: 10.1177/2047487318795189 journals.sagepub.com/home/ejpc Downloaded from https://academic.oup.com/eurjpc/article/25/14/1543/5926325 by guest on 13 September 2022