PROTEIN KINASE B SIGNALING PATHWAY IN EPICARDIAL ADIPOSE TISSUE FROM CORONARY PATIENTS

ANDRÉS NARVÁEZ PARDO; MIGUEL RUBIO; GABRIELA BERG; JULIETA CEBRÓN; GREGORIO FARIÑA; FERNANDO DOMINICI; MAGALI BARCHUK; JEANNIEL CAMPOS; LAURA SCHREIER

Mar del Plata

Congreso; REUNIÓN ANUAL DE SOCIEDADES DE BIOCIENCIAS 2022; 2022

Sociedad Argentina de Investigación Clínica

Cardiovascular disease (CVD) is the leading cause of mortality worldwide, despite the efforts of scientific community to find new causes and therapies for it. Directly related to CVD are obesity and insulin-resistance (IR), as main causes of the disease. In the last decades, epicardial adipose tissue (EAT), a visceral AT in direct contact with coronary arteries, has been proposed as an independent risk factor for CVD. We have previously reported a paradoxical behavior of EAT in IR, with an increase in Lipoprotein Lipase activity and its activators in coronary artery disease (CAD)-IR patients. To date, little is reported about insulin pathways in EAT. In this opportunity, our aim was to evaluate protein kinase B (AKT) activation as a step in insulin signaling pathway in EAT from CAD patients, and its association with IR markers. Materials and methods: we studied patients undergoing by-past graft surgery (CAD,n=10), and patients without CAD (No CAD,n=9). Serum lipoprotein and IR profiles were evaluated by colorimetric assays. In EAT and subcutaneous AT(SAT), we assessed Insulin Receptor (InR), AKT and Ser473-phospho-AKT (pAKT) expression by Western Blot. Results: despite higher IR markers in CAD, pAKT/AKT index was higher in EAT (p=0.02) and SAT (p=0.01) in this group compared to No CAD. pAKT/AKT index tended to be lower in EAT than SAT from the same group. No differences were found neither between groups nor tissues in InR levels (p>0.05). Conclusion: insulin pathway would be more activated in EAT from CAD patients, despite IR, highlighting the paradoxical behavior of the tissue. Nevertheless, the role of the different cell types in the tissue metabolism cannot be yet differentiated. These results may help guide future drug discoveries that target EAT for CAD prevention.