BIOMOLECULES OF ADIPOSE TISSUE IN ATHEROSCLEROTIC PLAQUES OF MEN WITH CORONARY ATHEROSCLEROSIS

Aim To study metabolic molecules (adiponectin, adipsin, resistin, glucagon-like peptide-1 (GLP-1), glucagon, secretin) of adipose tissue in atherosclerotic plaques (AP) and their associations with AP instability in men with coronary atherosclerosis. Material and methods Metabolic molecules (adipocytokines and metabolic hormones) of adipose tissue can act as enzymes, hormones or growth factors in modulating insulin resistance and lipid and glucose metabolism and indirectly influence the course of the atherosclerotic process. This study included 48 men from whom 139 coronary artery (CA) samples were collected during coronary artery bypass grafting, after obtaining the informed consent. According to the histological conclusion, 84 (60.4 %) CA plaques were stable, 44 (31.7 %) were unstable, and 11 histological samples had a conditionally unchanged CA intima (7.9 %). The concentrations of adiponectin, adipsin, resistin, GLP-1, glucagon, and secretin were measured in AP homogenates by multiplex analysis using the Human Metabolic Hormone V3 panel (MILLIPLEX, Germany). During the study, demographic and anthropometric characteristics, medical history, and presence of chronic diseases were recorded. Results The glucagon concentration in the conditionally unchanged intima was 16.7 % lower and in the fragments of unstable atherosclerotic plaques 41.2 % lower than in fragments of stable APs. However, the glucagon concentration in stable APs was 28 % higher than in unstable APs. The secretin concentration in the conditionally unchanged intima was also lower than in stable APs by 41.2 %, while in stable APs, the secretin concentration was 20 % higher than in unstable APs. The adiponectin concentrations were directly correlated with serum high-density lipoprotein cholesterol (HDL-C) concentrations (r=0.286; p=0.002), while the secretin concentrations were inversely correlated with serum HDL-C concentrations (r= -0.199; p=0.038). The probability of having an unstable AP (in relation to conditionally unchanged intima) increases by 35.8 % with an increase in the AP glucagon concentration by 1 pg / mg protein. The probability of having a stable AP (in relation to unchanged intima) increases by 29.4 % with an increase in the AP glucagon concentration by 1 pg / mg protein and by 10.1 % with an increase in the AP secretin concentration by 1 pg / mg protein. Conclusion The AP adiponectin concentration directly correlates and the AP secretin concentration inversely correlates with the serum concentration of HDL-C. The presence of both stable and unstable APs is directly associated with the AP glucagon concentration in men with coronary atherosclerosis. The AP secretin concentration is directly associated with plaque stability in men with coronary atherosclerosis. Further thorough study of the identified markers in atherosclerotic lesions will allow using them as potential targets for therapy.