Abstract
Epicardial adipose tissue (EAT) is an important risk factor for cardiovascular diseases (CVD). Recent clinical evidence suggested that the potential beneficial effects of glucagon‐like peptide 1 (GLP‐1) analogs on CVD may deal with the reduction of EAT amount, possibly by targeting EAT GLP‐1 receptor (GLP‐1R), as recently discovered. Nevertheless, the role of EAT GLP‐1R and its interplay with EAT genes involved in adipogenesis and fatty acids metabolism are presently unknown.
EAT was collected from 17 patients with coronary artery disease (CAD) undergoing elective coronary artery bypass graft for microarray analysis of GLP‐1R and genes involved in fatty acid metabolism and adipogenesis. GLP‐1 plasma levels were measured by enzyme‐linked immunosorbent assay. EAT thickness was measured by echocardiography. The study has been performed in accordance with the Principles of Declaration of Helsinki.
EAT GLP‐1R was directly correlated with genes promoting beta‐oxidation and white‐to‐brown adipocyte differentiation, and inversely with pro‐adipogenic genes. Circulating GLP‐1 levels were higher in CAD than healthy subjects and in patients with greater ultrasound‐measured EAT thickness.
GLP‐1 and its analogs may target EAT GLP‐1R and therefore reduce local adipogenesis, improve fat utilization and induce brown fat differentiation. The increase in circulating GLP‐1 levels may be a compensatory mechanism to improve metabolic dysfunctions. As EAT lies in direct contiguity to the myocardium and coronary arteries, the beneficial effects of GLP‐1 activation may extent to the heart.
Support or Funding Information
The study was supported by funding from Fondazione E. A. Fiera Internazionale di Milano to Università degli Studi di Milano and Ricerca Corrente funding from Italian Ministry of Health to IRCCS Policlinico San Donato.
This is from the Experimental Biology 2019 Meeting. There is no full text article associated with this published in The FASEB Journal.