Paraoxonase (PON1) activity in north west Indian Punjabis with coronary artery disease & type 2 diabetes mellitus.

ABSTRACT

BACKGROUND & OBJECTIVE: Paraoxonase (PON1), an arylesterase is associated with high density lipoprotein cholesterol (HDL-C). PON1 prevents low density lipo-protein cholesterol (LDL-C) from peroxidation and can also hydrolyze lipid peroxides, thereby providing protection against atherosclerosis and coronary artery disease (CAD). The incidence of CAD is known to be high in north western Indian Punjabis. Though many factors may play a role in its pathogenesis, low PON1 activity could be an independent risk factor. We carried out this study to determine PON1 activity in north-west Indian Punjabi patients with CAD with and without type 2 diabetes mellitus and compared with healthy individuals. METHODS: A total of 120 patients with angiographically proven CAD (57 with and 63 without type II diabetes mellitus) and 19 healthy controls were studied for plasma PON1 activity and lipid variables. Comparison was undertaken between CAD patients and healthy controls and between CAD patients with and without type II DM. RESULTS: Significantly lower plasma PON1 activity (P<0.05) along with lower HDL-C (P<0.001) and higher LDL-C (P<0.05) levels were observed in CAD patients as compared to healthy controls. On univariate analysis of variance after adjusting for age and sex, no significant difference could be observed between PON1 activity and age and sex. On discriminant analysis, no clear cut-off could be observed in PON1 activity between patients CAD and controls. Similarly between CAD with and without patients type II diabetes mellitus, there was no significant difference in PON1 activity and lipids. INTERPRETATION & CONCLUSION: The low plasma PON1 activity irrespective of being diabetic may be an independent risk factor for CAD in north-western Indian Punjabi population. Similar studies involving larger samples in different ethnic groups in India need to be done to find out the role of PON1 activity in CAD.