Serum paraoxonase activity in patients with type 1 diabetes compared to healthy controls

Eur J Clin Invest. 2002 Apr;32(4):259-64. doi: 10.1046/j.1365-2362.2002.00977.x.

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.

Design: 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.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Arteriosclerosis / pathology
  • Aryldialkylphosphatase
  • Diabetes Mellitus, Type 1 / enzymology*
  • Disease Progression
  • Esterases / blood*
  • Esterases / genetics
  • Female
  • Humans
  • Lipoproteins, HDL / metabolism
  • Lipoproteins, LDL / metabolism
  • Male
  • Polymorphism, Genetic

Substances

  • Lipoproteins, HDL
  • Lipoproteins, LDL
  • Esterases
  • Aryldialkylphosphatase
  • PON1 protein, human