ECE2023 Poster Presentations Diabetes, Obesity, Metabolism and Nutrition (159 abstracts)
1INFIBIOC, Faculty of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina; 2National Institute of Health and Medical Research (INSERM), Marseille, France; 3Teaching and Research Service, Formosa Central Hospital, National University of Formosa, Formosa, Formosa, Argentina; 4Division of Cardiovascular Surgery, Hospital de Clínicas José de San Martín, University of Buenos Aires, Buenos Aires, Argentina
Ceramides (Cer), which are known to be altered in plasma before the onset of coronary artery disease (CAD), have been proposed as new markers for cardiovascular disease (CVD) risk. Serum Cer18:1/C16:0, Cer18:1/C18:0 and Cer18:1/C24:1 to Cer18:1/24:0 indexes are proposed to be indicative of CAD. Epicardial adipose tissue (EAT) is a visceral adipose tissue, surrounding and in direct contact with the myocardium and coronary arteries, which volume is considered a risk factor for CVD. Studies from our laboratory demonstrated an increase in EAT Cer total content from CAD patients. We also reported an increase in Lipoprotein Lipase (LPL) activity in EAT from CAD and Diabetes Mellitus 2 (DM2) patients, suggesting that LPL would be involved in EAT expansion. EAT Cer content was directly associated with LPL activity. Our aim was to evaluate the association between EAT Cer indexes and LPL activity, and markers of EAT lipid metabolism, in CAD patients with and without DM2.
Methods: Patients undergoing coronary by-pass graft (CAD, n=24), with and without DM2 (DM2, n=7; No-DM2, n=17), and patients without CAD (noCAD, n=13) were studied. In EAT, LPL activity, Angiopoietin-like protein 4, Glycosylphosphatidylinositol anchored high density lipoprotein binding protein-1 (GPIHBP1), Peroxisome Proliferator Activated Receptor γ (PPARγ), VLDL-Receptor(R) and Fatty Acid Binding Protein-4 expression were assessed. Tissue lipidome was evaluated by UHPLC-MS.
Results: CAD-DM2 patients presented a deleterious and atherogenic metabolic profile compared to the other groups. CAD-No DM2 and CAD-DM2 presented a higher Cer18:1/C24:1 to Cer18:1/24:0 index than noCAD (P=0.017 and P=0.003 respectively), with no differences between CAD diabetic and CAD no diabetic patients. This index was directly associated with LPL activity (r=0.373, P=0.042), PPARγ (r=0.637, P=0.009), GPIHBP1 (r=0.497, P=0.18) and VLDL-R (r=0.441, P=0.031). No differences were found among groups neither in Cer18:1/C16:0 nor Cer18:1/C18:0 to Cer18:1/24:0 indexes.
Conclusion: This is the first time that a relation between LPL, its regulators and Cer is reported in AT. EAT Cer indexes could be suggested as markers of the tissue metabolism in CAD and DM2.