Balkan Journal of Medical Genetics

ROLE OF THE APOB GENE POLYMORPHISM (c.12669G>A, p.Gln4154Lys) IN CORONARY ARTERY DISEASE IN THE INDIAN PUNJABI POPULATION
Sharma R1,*, Mahajan M2, Singh B1, Singh G3, Singh P3
*Corresponding Author: Ritu Sharma, Department of Biochemistry, Government Medical College, Circular Road, Amritsar-143001, Punjab, India; Tel.: +91-183-257-3637; Fax: +91-183-242-6506: E-mail: ritu_gmc@ rediffmail.com
page: 35

RESULTS

The subjects under study had either the R+R+ genotype or R+R– genotype. No individual with homozygous mutant alleles, i.e., R–R–, was identified (Figure 1). The frequency of R+ and R– alleles was calculated (with an allele counting method) in control subjects as well as in CAD patients. The frequency of the R– allele was significantly higher (p <0.05) in CAD patients when compared to controls. In order to study the association of the R– allele with CAD, variations in serum lipids, lipoprotein cholesterol and apoB levels of CAD patients and control subjects with different apoB genotypes were investigated (Table 1). Total cholesterol, triglycerides, very low-density lipo-protein-cholesterol (VLDL-C), lowdensity lipoprotein-cholesterol (LDL-C) and highdensity lipoprotein-cholesterol (HDL-C) levels did not differ significantly in the subjects, whether they were CAD patients or controls carrying the R+R+ or R+R– APOB genotype. The data were analyzed after segregating subjects on the basis of age and gender. However, CAD patients with the R+R– genotype had significantly raised (p <0.05) serum apoB levels as compared to those having the R+R+ genotype. Raised serum apoB levels indicate the predominance of small dense LDL particles that are more prone to oxidation. The MDA-LDL levels and apoB carbonyl content of LDL did not differ significantly in CAD patients with different APOB genotypes (Table 2). A similar trend was observed in Log triglyceride/ high-density lipoprotein-cholesterol (HDL-C) value which was taken as an index of LDL particle size. Overall, CAD patients had increased predominance of small dense LDL particles resulting in their increased oxidation. However, this observation was independent of APOB genotypes.

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