Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. Serum levels of novel adipokines, omentin-1 and chemerin, in patients with acute myocardial infarction: KOZANI STUDY Nikolaos P.E. Kadoglou a,b , Dimitrios K. Tahmatzidis b , Christos Giannakoulas b , Alkistis Kapelouzou c , Argirios Gkontopoulos b , John Parissis a , Stylianos Lampropoulos b and George Kottas b Objectives The role of the novel adipokines, omentin-1 and chemerin, in coronary artery disease is still obscure. The present study analyzed the serum levels of omentin-1 and chemerin in patients with acute myocardial infarction (AMI) as well as prospectively 6 months post-AMI. Methods Seventy-eight patients (63 men and 15 women) with first AMI were enrolled. Thirty-two age-matched and sex-matched individuals without overt cardiovascular disease served as healthy controls. Serum levels of omentin-1, chemerin, interleukin-18 (IL-18), high-sensitivity C-reactive protein (hsCRP), glycemic and lipid profiles, blood pressure, BMI and ejection fraction were assayed. In AMI patients, blood samples were obtained at hospital admission and after 6 months, whereas coronary angiography was performed within 7 days after admission. Results At baseline, AMI group appeared with significantly lower ejection fraction, omentin-1 and high-density lipoprotein serum levels, whereas it had higher concentrations of white blood cells count (WBC), hsCRP, IL-18 and chemerin compared with healthy controls (P < 0.05). After 6 months of follow-up, the concentrations of WBC, hsCRP and IL-18 significantly downregulated, whereas omentin-1 levels considerably increased (from 18.73 W 3.66ng/ml to 28.62 W 5.61 ng/ml, P < 0.001) within AMI group. In contrast, serum chemerin did not significantly change (263.37 W 73.32ng/ml vs. 195.90 W 84.32 ng/ml, P U 0.190). In standard multiple regression analyses, baseline levels and changes of hsCRP and IL-18 levels during follow-up remained independent determinants of omentin-1, respectively at baseline and after follow-up. Conclusion Patients with AMI showed at admission lower omentin-1 and higher chemerin serum levels compared with healthy controls. The suppression of inflammation in the 6-month post-AMI period might have mediated the significant upregulation of omentin-1, implicating a novel target of treatment. J Cardiovasc Med 2015, 16:341–346 Keywords: adipokines, chemerin, coronary artery disease, myocardial infarction, omentin-1 a 2nd Department of Cardiology, ‘Attikon’ University Hospital, Athens, b Department of Cardiology, ‘Mamatsio’ General Hospital, Kozani and c Center of Experimental Surgery, Biomedical Research Foundation, Academy of Athens, Greece Correspondence to Nikolaos P.E. Kadoglou, 124 Vosporou str, GR-54454 Thessaloniki, Greece Tel: +30 2310905178; fax: +30 2310905178; e-mail: nikoskad@yahoo.com, nkado@med.uoa.gr Received 3 June 2013 Revised 18 February 2014 Accepted 18 February 2014 Introduction Acute myocardial infarction (AMI) represents the most detrimental clinical manifestation of coronary artery dis- ease (CAD), induced by plaque rupture. The latter is a complex inflammatory response of the vessel wall ignited by activated macrophages and T cells, leading to proteo- lytic degradation of connective tissue matrix, excessive production of proinflammatory cytokines and apoptosis of vascular cells. 1 The mediating role of inflammation in plaque destabilization is widely accepted. Adipose tissue secretes various bioactive, proinflamma- tory cytokines, known as adipokines. Those adipose tissue derivatives are usually upregulated in the adiposity state and seem to mediate most atherosclerosis-related complications. 2 The novel fat-depot cytokine, omentin, was first identified in omental human adipose tissue. 3 Decreased levels of omentin-1 are associated with increasing obesity and insulin-resistance state, such as diabetes. 4 Recent data support the independent associ- ation of low circulating omentin-1 levels with arterial stiffness, a valid cardiovascular prognostic factor, and carotid atherosclerosis in patients with type 2 diabetes mellitus (T2DM). 5 Moreover, recent evidence suggests the inverse relationship of omentin-1 with CAD presence and severity. 6 However, no data are still available regard- ing the possible role of omentin-1 in the long-term after acute coronary syndromes (ACS). Chemerin is an agonist of the orphan G-protein-coupled receptor chemokine-like receptor 1 (CMKLR1 and ChemR23), which modulates adipocytes differentiation 7 and seems to link obesity and inflammation. 8 In healthy individuals, plasma chemerin levels are significantly associated with BMI, circulating triglycerides and blood pressure (BP), suggesting a strong relationship of this Original article 1558-2027 Copyright ß 2015 Wolters Kluwer Health, Inc. All rights reserved. DOI:10.2459/JCM.0000000000000053