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Deleterious effect of glycation on the ability of HDL to counteract the inhibitory effect of oxidized LDL on endothelium‐dependent vasorelaxation
Author(s) -
Brindisi M. C.,
Duvillard L.,
Monier S.,
Vergès B.,
Perségol L.
Publication year - 2013
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/dmrr.2434
Subject(s) - glycation , medicine , endocrinology , chemistry , fructosamine , incubation , apolipoprotein b , lipoprotein , vasodilation , low density lipoprotein , endothelium , high density lipoprotein , cholesterol , diabetes mellitus , biochemistry
Background Contrary to high‐density lipoprotein (HDL) from normolipidaemic and normoglycaemic subjects, HDL from diabetic patients loses its ability to reverse the inhibition of vasorelaxation induced by oxidized low‐density lipoprotein (LDL). The aim of this study was to analyze the role of glycation, a major abnormality observed in diabetes, on the impairment of the vasorelaxant effect of HDL. Methods HDL from healthy subjects was glycated in vitro by incubation in glucose 200 mmol/L for 3 days. Vasoreactivity was evaluated by the relaxation response to acetylcholine of rabbit aorta rings pre‐contracted with noradrenaline, before and after 2 h incubation with or without different lipoprotein fractions (Krebs buffer, oxidized LDL, normal or glycated HDL alone and with oxidized LDL). Result The fructosamine/apolipoprotein AI ratio was significantly increased in glycated HDL compared with native HDL (53.63 ± 7.91 vs 18.51 ± 4.10 µmol/g; p < 0.05). Oxidized LDL inhibited endothelium‐dependent vasodilation compared with Krebs buffer [maximal relaxation (Emax) = 53.15 ± 6.50 vs 98.67 ± 2.07%, p < 0.001]. Native HDL was able to counteract the oxidized LDL‐induced inhibition of vasorelaxation (Emax = 76.93 ± 5.41 vs 53.15 ± 6.50%, p < 0.001). On the other hand, glycated HDL had no effect on oxidized LDL‐induced inhibition of endothelium vasorelaxation compared with incubation with oxidized LDL alone (Emax = 52.98 ± 2.07 vs 53.15 ± 6.50%, not significant). Conclusion Glycation of HDL induces the loss of the ability of HDL to counteract the inhibitory effect of oxidized LDL on endothelium‐dependent vasorelaxation, this is likely contributing to the impairment of antiatherogenic properties of HDL in diabetic patients. Copyright © 2013 John Wiley & Sons, Ltd.