Aleš Smékal1, Jan Václavík2, David Stejskal3, Klára Benešová4, Jiří Jarkovský4, Gabriela Svobodová5, Radmila Richterová6, Marek Švesták5, Miloš Táborský1. 1. Department of Internal Medicine I - Cardiology, University Hospital Olomouc and Faculty of Medicine and Dentistry, Palacky University Olomouc, Czech Republic. 2. Department of Internal Medicine I - Cardiology, University Hospital Olomouc and Faculty of Medicine and Dentistry, Palacky University Olomouc, Czech Republic. Electronic address: vaclavik.j@centrum.cz. 3. AGEL Research and Training Institute, Prostejov, Czech Republic; Institute of Medical Chemistry and Biochemistry, Faculty of Medicine and Dentistry, Palacky University Olomouc, Czech Republic; Department of Biomedical Sciences, Faculty of Medicine, Ostrava University, Czech Republic. 4. Institute of Biostatistics and Analyses at the Faculty of Medicine and the Faculty of Science of the Masaryk University, Brno, Czech Republic. 5. AGEL Research and Training Institute, Prostejov, Czech Republic; Institute of Medical Chemistry and Biochemistry, Faculty of Medicine and Dentistry, Palacky University Olomouc, Czech Republic. 6. Agel Laboratories, Novy Jicin, Czech Republic.
Abstract
OBJECTIVES: Little is known about the role of adipokines in the pathogenesis of coronary artery disease in young patients. The aims of this study were to compare serum levels of adipokines and expression of adipokines in peripheral blood leukocytes in patients with premature coronary artery disease (CAD), metabolic syndrome and healthy individuals. DESIGN AND METHODS: Sixty-five patients with premature CAD (men 18-45years old and women 18-55years old) formed the study group. The control groups were 75 patients with metabolic syndrome and 50 healthy individuals. For each group, RNA expression in peripheral blood leukocytes was determined for 24 different adipokines and 11 adipokines were examined in serum. RESULTS: In individuals with CAD, serum visfatin levels were significantly higher than in metabolic syndrome and healthy controls (2.3 vs. 1.6 vs. 0.7µg/L, P<0.001) while both omentin-1 (92.9 vs. 587.0 vs. 552.3µg/L, P<0.001) and ZAG2 (45.5 vs. 72.5 vs. 77.1mg/L, P<0.001) levels were lower. The receiver operating curve (ROC) analysis for testing the validity of these adipokines in the diagnosis of CAD compared to control groups provided the following areas under the curve (AUC): omentin-1 AUC 0.97 (cut-off ≤222µg/L), ZAG2 AUC 0.89 (cut-off ≤51.7mg/L) and visfatin AUC 0.74 (cut-off ≥1.0µg/L) (P<0.001 in all cases). Visfatin and omentin-1 serum levels did not differ between the acute phase of myocardial infarction and the chronic phase of CAD. In patients with CAD, we found no significant relation between mRNA expression and adipokine concentration. CONCLUSION: Serum omentin-1, visfatin and ZAG2 could serve as biomarkers of premature CAD in young apparently healthy people.
OBJECTIVES: Little is known about the role of adipokines in the pathogenesis of coronary artery disease in young patients. The aims of this study were to compare serum levels of adipokines and expression of adipokines in peripheral blood leukocytes in patients with premature coronary artery disease (CAD), metabolic syndrome and healthy individuals. DESIGN AND METHODS: Sixty-five patients with premature CAD (men 18-45years old and women 18-55years old) formed the study group. The control groups were 75 patients with metabolic syndrome and 50 healthy individuals. For each group, RNA expression in peripheral blood leukocytes was determined for 24 different adipokines and 11 adipokines were examined in serum. RESULTS: In individuals with CAD, serum visfatin levels were significantly higher than in metabolic syndrome and healthy controls (2.3 vs. 1.6 vs. 0.7µg/L, P<0.001) while both omentin-1 (92.9 vs. 587.0 vs. 552.3µg/L, P<0.001) and ZAG2 (45.5 vs. 72.5 vs. 77.1mg/L, P<0.001) levels were lower. The receiver operating curve (ROC) analysis for testing the validity of these adipokines in the diagnosis of CAD compared to control groups provided the following areas under the curve (AUC): omentin-1 AUC 0.97 (cut-off ≤222µg/L), ZAG2 AUC 0.89 (cut-off ≤51.7mg/L) and visfatin AUC 0.74 (cut-off ≥1.0µg/L) (P<0.001 in all cases). Visfatin and omentin-1 serum levels did not differ between the acute phase of myocardial infarction and the chronic phase of CAD. In patients with CAD, we found no significant relation between mRNA expression and adipokine concentration. CONCLUSION: Serum omentin-1, visfatin and ZAG2 could serve as biomarkers of premature CAD in young apparently healthy people.
Authors: Fernanda Genre; Javier Rueda-Gotor; Sara Remuzgo-Martínez; Verónica Pulito-Cueto; Alfonso Corrales; Verónica Mijares; Leticia Lera-Gómez; Virginia Portilla; Rosa Expósito; Cristina Mata; Ricardo Blanco; Javier Llorca; Vanesa Hernández-Hernández; Esther Vicente; Cristina Fernández-Carballido; María Paz Martínez-Vidal; David Castro-Corredor; Joaquín Anino-Fernández; Carlos Rodríguez-Lozano; Oreste Gualillo; Juan Carlos Quevedo-Abeledo; Santos Castañeda; Iván Ferraz-Amaro; Raquel López-Mejías; Miguel Á González-Gay Journal: Sci Rep Date: 2020-06-15 Impact factor: 4.379