INVESTIGADORES
DOMINICI Fernando Pablo
congresos y reuniones científicas
Título:
PROTEIN KINASE B SIGNALING PATHWAY IN EPICARDIAL ADIPOSE TISSUE FROM CORONARY PATIENTS
Autor/es:
BARCHUK M ; CEBRÓN J; NARVAEZ PARDO A; CAMPOS J; FARIÑA G; RUBIO M; SCHREIER L; DOMINICI F; BERG G
Reunión:
Congreso; LXVII REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA (SAIC); 2022
Resumen:
Cardiovascular disease (CVD) is the leading cause of mortalityworldwide, despite the efforts of scientific community to find newcauses and therapies for it. Directly related to CVD are obesity andinsulin-resistance (IR), as main causes of the disease. In the lastdecades, epicardial adipose tissue (EAT), a visceral AT in direct contact with coronary arteries, has been proposed as an independentrisk factor for CVD. We have previously reported a paradoxical behavior of EAT in IR, with an increase in Lipoprotein Lipase activityand its activators in coronary artery disease (CAD)-IR patients. Todate, little is reported about insulin pathways in EAT. In this opportunity, our aim was to evaluate protein kinase B (AKT) activation asa 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.