The aim of this study was to determine whether the
paraoxonase (PON1) status, i.e. PON1 activities and phenotypes (AA, AB and BB), and its relationship with
lipid status are different in patients with type II diabetes as compared to healthy population. Diabetic group comprised 175 patients with type II
diabetes mellitus (94 men and 81 women) who came to their regular control examination and took the oral
glucose tolerance test. Patients with type II
diabetes mellitus diagnosis for 12 years on average were on peroral
antidiabetics, or
insulin or diet, and 3 patients had no
therapy prescribed yet. Control group comprised 114 apparently healthy individuals (28 men and 86 women) who were not on any medication. The
paraoxonase activity was measured with 2.0 mmol L(-1)
paraoxon in the absence and in the presence of 1.0 mol L(-1) NaCl, and with 2.0 mmol L(-1)
phenylacetate. Both activities were measured spectrophotometrically at 37 degrees C in 0.1 mol L(-1) Tris-HCl
buffer, pH = 8.0, containing 2.0 mmol L(-1) CaCl(2). Sera of diabetic and control subjects were assigned to the
paraoxonase phenotypes on the basis of the basal
paraoxonase activity distribution. We assigned 45% sera of male and 49% sera of female diabetic patients, and 64% sera of both genders of the control group to the AA low activity phenotype. There were no differences in
paraoxonase activities between the gender- and phenotype-matched diabetic and control groups.
Enzyme activity against the
phenylacetate was higher, and phenotype-dependent, only in diabetic patients. In contrast to AA phenotype individuals, total
cholesterol and
LDL-cholesterol in the female diabetic group and
triglyceride concentration in the male diabetic group assigned to pooled AB and BB phenotypes were higher than in the corresponding controls. It follows from PON1 phenotype distribution that less antiatherogenic
paraoxonase B allele is more frequent in type II
diabetes mellitus than in the healthy population. Their
lipid status is more atherogenic, which could indicate a risk of premature
atherosclerosis.