title: HDL particles from type 1 diabetic patients are unable to reverse the inhibitory effect of oxidised LDL on endothelium-dependent vasorelaxation.
abstract: OBJECTIVE
  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 micromol/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
  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.
authors.affiliation: INSERM Research Center 866, Dijon, France.
authors.forename: L
authors.initials: L
authors.lastname: Perségol
authors.forename: M
authors.initials: M
authors.lastname: Foissac
authors.forename: L
authors.initials: L
authors.lastname: Lagrost
authors.forename: A
authors.initials: A
authors.lastname: Athias
authors.forename: P
authors.initials: P
authors.lastname: Gambert
authors.forename: B
authors.initials: B
authors.lastname: Vergès
authors.forename: L
authors.initials: L
authors.lastname: Duvillard
mesh_terms: D000328:Adult; D000818:Animals; D043303:Aryldialkylphosphatase / Q000097:blood / Q000494:pharmacology; D003922:Diabetes Mellitus, Type 1 / Q000097:blood*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood* / Q000494:pharmacology*; D008077:Lipoproteins, LDL / Q000097:blood / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D011817:Rabbits; D012016:Reference Values; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
chemical_list: D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; D043303:Aryldialkylphosphatase