Abstract 15066: Lipid Transfer to Hdl in Type 2 Diabetic Patients With and Without Coronary Artery Disease
Background: Assuming that in type 2 diabetes mellitus (DM2), the HDL-cholesterol is reduced and this may interfere with the genesis of atherosclerosis, the understanding of existing functional and metabolic changes is important to establish its influence in diabetic patients without coronary artery disease (CAD).
In this scenario the lipid transfers to HDL are crucial steps in the formation of HDL and its role in reverse cholesterol transfer.
Objective: Investigate whether the emergence of CAD in patients with DM2 are associated with changes in lipid transfer to HDL and in content of free cholesterol in the plasma.
Methods: We studied 165 diabetic patients (85 with CAD and 80 without CAD). Demographic, clinical, laboratory, and time of the existence of diabetes were similar for both groups. Plasma was incubated for 1h at 37oC with a donor nanoemulsion labeled with 3H-cholesteryl-esters and14C-phospholipids or with 14C-free cholesterol-and 3H-triglycerides. Radioactive lipids Transferred from the donor nanoemulsion to HDL were measured in the supernatant after chemical precipitation of non-HDL fractions and the nanoemulsion. Results are% of the total radioactivity of each lipid in HDL.
Results: In DM2-CAD, total cholesterol, LDL-cholesterol and apoB were higher than in DM2. Compared to DM2, DM2-CAD showed diminished transfer to HDL of free-cholesterol (DM2-CAD=7.6 ± 1.2; DM2= 8.1±1.5%, p=0, 01) and of cholesteryl-ester (4.0 ± 0.6 vs 4.3 ± 0.7,p<0.01). Plasma free-cholesterol was higher in DM2-CAD (DM2-CAD=36.8 ± 8.1; DM2=34.4 ± 7.1, p=0.04) and CETP concentration was diminished (2.5 ± 1.1 vs 2.1 ± 1.0, p=0.02).LCAT activity, HDL particle diameter and lipid composition was equal in both groups.
Conclusion: The reduction of free-cholesterol transfer to HDL may impair cholesterol esterification and reverse cholesterol transport. Those disturbances in HDL metabolism may facilitate the emergence of CAD in DM2.
- © 2013 by American Heart Association, Inc.