Relationship between cardiovascular risk factors and adipocytokines gene expression in local fat depots

Abstract

Abstract In this study we studied the relationships between adipokines (leptin, soluble leptin receptor) in adipose tissue (AT) and cardiovascular disease (CVD) risk factors. Methods Fat tissue biopsies were obtained from 134 patients median aged 64.0 (48.0; 68.0) with stable CAD undergoing coronary artery bypass grafting. Traditional cardiovascular risk factors and patient treatment have been recorded. AH was defined as systolic blood pressure >140 mm Hg Art., diastolic blood pressure >90 mm Hg. Dyslipidemia was defined as a previously detected increase in total serum cholesterol (>200 mg/dl), triglycerides (>200 mg/dl), or low-density lipoprotein (LDL) cholesterol (>150 mg/dl) for at least 1 year, or use of lipid-lowering drugs. Smoking was classified as current or former smokers; current smoking status was defined as at least one cigarette daily over the last year. Adipocytes were isolated from subcutaneous (SAT), epicardial (EAT), and perivascular AT (PVAT) samples. Isolated adipocytes were cultured for 24-h after which, Then adipocytes were immediately processed to RNA extraction and determination of adipokines gene expression. Results In this study, we showed that men with CAD LEP and LEPR expression were lower in PVAT, whereas only the latter was decreased in SAT. Thus, LEPR expression in local fat depots appeared to differ in men and women, which is consistent with previous reports. Men with CAD showed lower LEP expression than women in EAT, whereas no significant differences were observed in SAT. Patients 51–59 years old were characterized by the lowest LEP expression in SAT and the highest LEP and LEPR expression in EAT and PVAT. Those >60 years presented the highest levels of LEPR in SAT. The presence of dyslipidemia in patients with CAD correlated with decreased LEPR expression in EAT, which is an unfavorable sign and may potentially lead to the development of leptin resistance. In patients with AH, LEP expression in EAT and LEPR expression in SAT and PVAT is increased. AH >20 years was associated with increased LEP in ATs. Smokers with CAD exhibited higher levels of LEP expression in SAT and EAT, and LEPR expression in SAT. Conclusions The results of the study indicate a close association of traditional CVD risk factors with adipocytokine imbalance in patients with CAD. The results indicate the potential of the fat depot and leptin and its receptor data as a drug application point. The study of the molecular basis of PVAT and EAT function can provide a more complete understanding of the etiopathogenetic mechanisms of CVD and develop an effective strategy for their prevention and control. Funding Acknowledgement Type of funding sources: None.