title: Serum paraoxonase activity in patients with type 1 diabetes compared to healthy controls.
abstract: BACKGROUND
  The oxidation of low-density lipoprotein (LDL) is central to current theories on the initiation and progression of atherosclerosis. Type 1 diabetes is associated with an increase in oxidative stress, which may be responsible for the increased susceptibility to coronary heart disease seen in type 1 diabetes. High-density lipoprotein (HDL) associated paraoxonase (PON1) can retard the oxidation of LDL.
  
  
  METHODS
  Paraoxonase activity, concentration and genotype were therefore investigated in 152 people with type 1 diabetes and 282 healthy controls. These parameters were also investigated in the group with type 1 diabetes in relation to the presence of diabetic complications.
  
  
  RESULTS
  Both PON1 activity and concentration were significantly lower by 16.7% and 19.2% (both P < 0.05) in the type 1 diabetes group. These differences were independent of the PON1 coding region polymorphisms. The distribution of PON1 activity and mass were the same in both populations, i.e. for the PON1-192 polymorphism RR > RQ > QQ and for the PON1-55 polymorphism LL > LM > MM. There were no differences in either the PON1 polymorphisms, PON1 activity and concentration in people with type 1 diabetes in the presence or absence of micro and macro vascular complications of diabetes.
  
  
  CONCLUSIONS
  Low PON1 activity may contribute to the increased atherosclerosis found in type 1 diabetes by reducing the ability of HDL to retard LDL oxidation despite the frequently-found increased HDL in type 1 diabetes when good glycaemic control is established.
authors.affiliation: University Department of Medicine, Manchester Royal Infirmary, Manchester, UK.
authors.forename: B
authors.initials: B
authors.lastname: Mackness
authors.forename: P N
authors.initials: PN
authors.lastname: Durrington
authors.forename: A J M
authors.initials: AJ
authors.lastname: Boulton
authors.forename: D
authors.initials: D
authors.lastname: Hine
authors.forename: M I
authors.initials: MI
authors.lastname: Mackness
mesh_terms: D000328:Adult; D001161:Arteriosclerosis / Q000473:pathology; D043303:Aryldialkylphosphatase; D003922:Diabetes Mellitus, Type 1 / Q000201:enzymology*; D018450:Disease Progression; D004950:Esterases / Q000097:blood* / Q000235:genetics; D005260:Female; D006801:Humans; D008075:Lipoproteins, HDL / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D011110:Polymorphism, Genetic
chemical_list: D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D004950:Esterases; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human