HDL particles from type 1 diabetic patients are unable to reverse the inhibitory effect of oxidised LDL on endothelium-dependent vasorelaxation |
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Authors: | L Perségol M Foissac L Lagrost A Athias P Gambert B Vergès L Duvillard |
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Institution: | (1) INSERM Research Center 866, Dijon, France;(2) University of Burgundy, IFR 100, Dijon, France;(3) Department of Endocrinology and Metabolic Diseases, CHU Dijon Bocage Hospital, Dijon, France;(4) Department of Medical Biochemistry, CHU Dijon Bocage Hospital, P.O. Box 77908, 21079 Dijon Cedex, France |
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Abstract: | Aims/hypothesis In healthy individuals, HDL can counteract the inhibition of vasorelaxation induced by oxidised LDL. Several abnormalities
such as increased size, glycation and decreased paraoxonase activity have been reported for HDL from type 1 diabetic patients.
Thus, we hypothesised that the ability of HDL to protect vessels against impairments of vasorelaxation would be decreased
in these patients.
Methods We compared the ability of HDL from 18 type 1 diabetic patients and 12 control participants to counteract the inhibition of
endothelium-dependent relaxation induced by oxidised LDL on rabbit aorta rings.
Results Serum triacylglycerol and total cholesterol, LDL- and HDL-cholesterol were similar in type 1 diabetic and control participants.
Fasting glycaemia and the HDL-fructosamine level were higher in diabetic patients than in controls (9.06 ± 3.55 vs 5.27 ± 0.23 mmol/l,
p < 0.005; and 10.2 ± 3.2 vs 7.7 ± 2.5 μmol/g protein, p < 0.05, respectively). HDL composition, size and paraoxonase activity were similar in both groups. HDL from controls reduced
the inhibitory effect of oxidised LDL on maximal relaxation (E
max; 79.3 ± 11.8 vs 66.4 ± 11.7%, p < 0.05), whereas HDL from type 1 diabetic patients had no effect (E
max = 70.6 ± 17.4 vs 63.9 ± 17.2%, NS). In type 1 diabetic patients, E
max was not correlated with glycaemia or the HDL-fructosamine level.
Conclusions/interpretation HDL particles from type 1 diabetic patients do not protect against inhibition of endothelium-dependent vasorelaxation induced
by oxidised LDL, in contrast to HDL particles from healthy individuals. This defect cannot be explained by abnormalities in
HDL composition, size or paraoxonase activity, and may contribute to the early development of atherosclerotic lesions in type
1 diabetic patients.
L. Perségol and M. Foissac contributed equally to this study. |
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Keywords: | Aorta rings Endothelium-dependent vasorelaxation HDL Oxidised LDL Rabbit Type 1 diabetes mellitus |
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