Association of the lipoprotein lipase and Apolipoprotein C-II gene polymorphisms with risk of dyslipidemia in smokers and non-smokers male.

OBJECTIVE

Dyslipidaemia is considered a metabolic abnormality andan important risk factor that leads to atherogenic cardiovascular diseases. Cigarette smoking is associated with dyslipidaemia. This study aimed to demonstrate whether lipoprotein lipase enzyme (LPL) and Apolipoprotein CII (APOCII) gene polymorphisms can be considered as independent genetic risk factors for dyslipidaemia among smokers with various smoking durations.

METHODS

A total of 185 males (90 smokers and 95 non-smokers)were included in this study, Lipid profiles were measured and DNA was isolated. The LPL-Hind III and APO CII-Ava II polymorphisms were determined using the polymerase reaction-restriction fragment length polymorphisms (RFLP) technique.

RESULTS

For the LPL-Hind IIIpolymorphism H+H+ genotype group, the triglycerides TG and very-low-density lipoprotein cholesterol VLDL-C concentrations were significantly higher and the high-density lipoprotein cholesterol HDL-C concentration was significantly lower than those of the H-H- genotype. ForAPO CII-Ava II polymorphisms, compared with those of the A2A2 genotype group, the total cholesterol TC, TG, low-density lipoprotein cholesterol LDL-C and VLDL-C concentrations were significantly increased in the A1A2 genotype group, while the HDL-C concentration was significantly decreased.

CONCLUSIONS

The study revealed that the H+H+ or H + H-genotype of the LPL-Hind III polymorphism and the A1A1or A1A2 genotype of the APOCII-Ava II polymorphism were at higher risk of developing dyslipidaemia compared to the H-H- genotype of the LPL-Hind III polymorphism and A2A2 genotype of the APOCII-Ava II polymorphism.