LIPOPROTEIN LIPASE ACTIVITY IS ENHANCED IS EPICARDIAL ADIPOSE TISSUE FROM DIABETIC PATIENTS.

BARCHUK, MAGALI; MIKSZTOWICZ, VERONICA; FERNANDEZ TOME, MARÍA DEL CARMEN; RUBIO, MIGUEL; LOPEZ, GRACIELA; SCHREIER , LAURA; BERG, GABRIELA

Congreso; IV INTERNATIONAL CONGRESS IN TRANSLATIONAL MEDICINE; 2018

Obesity and its associated co-morbidities, such as Type-2 Diabetes Mellitus (T2DM) are increasing worldwide, together with an increased risk of cardiovascular diseases (CVD). Epicardial Adipose tissue (EAT) is a visceral adipose tissue, which surrounds and infiltrates myocardium and coronary arteries. It has been demonstrated than EAT expansion is associated to an increased risk of CVD. Lipoprotein Lipase (LPL) is the major enzyme involved in triglycerides (TG) hydrolysis from circulating TG-rich lipoproteins (Chylomicrons and VLDLs), supplying fatty acids to AT and contributing to its expansion. This enzyme is highly regulated at both transcriptional (PPARs receptors) and post-translational (Angiopoietin-like proteins, ANGPTLs) levels. It is known that EAT volume is higher in T2DM patients compared to No T2DM patients, although there are no reports about LPL activity in this tissue, and the possible contribution to its expansion. In this context, our aim was to evaluate LPL activity in EAT from T2DM and No T2DM patients. We also studied PPARγ and ANGPTL4 expression, and EAT LPL contribution to circulating VLDL characteristics.Materials and Methods: we studied 43 patients with coronary artery disease, undergoing by-pass graft, divided into two groups: T2DM group (n=16) and No T2DM group (n=27). Anthropometric measures and serum metabolic profile were assessed before surgery, TG/HDL-cholesterol index was calculated to asses Insulin Resistance (IR). During surgery, EAT and Subcutaneous AT (SAT) were obtained. LPL activity was evaluated by a radiometric assay, and regulators expression was determined by western blot. Circulating VLDL were isolated by ultracetrifugation, and characterized in lipid and protein content.Results: Glucose was higher in T2DM patients (p=0.03), without differences in lipoprotein profile between groups. EAT LPL activity was higher in T2DM than in No T2DM (p=0.05), even after adjusting for metformin treatment, and it was negatively associated to TG levels (r=-0.446, p=0.01) and TG/HDL-chol index (r=-0.590, p=0.001), without differences in SAT LPL activity. In both groups, LPL activity was higher in EAT than in SAT (p