Association between ApoE Gene Polymorphism and Serum Lipid Profile in Coronary Heart Disease and Healthy Subjects

Abstract

Apolipoprotein E (ApoE) plays a role in the regulation of the lipid metabolism of humans. ApoE, 229 amino acid polypeptide, is classified into three major isoforms (E2, E3, E4) according to the differences of amino acid in positions 112 and 158. In the normal population ApoE3 isoform is the most prevalent and ApoE2 or E4 are frequently associated with hyperlipoproteinemia. The objective of this study was to investigate the relationship between ApoE gene polymorphism and serum lipid profile and coronary heart disease (CHD) in Gaza Strip. Methods: Polymerase chain reaction-restricted fragments length polymorphism (PCR-RFLP) was used to determine ApoE genotypes using the two restrictionenzymes; AflIII (A) and HaeII (H). Our study population consisted of 137 subjects including 69 cases (45 male, 24 female) CHD and 68 (33 male and 35 female) healthy subjects. Two blood samples were collected from each subject one was whole blood and the other was serum after fasting for 12-16 hours. Results: the ApoE3/E3 genotype was the most common in the control and the CHD groups. ApoE2/E3 and ApoE4/E3 were the next most common genotypes. The frequencies of ApoE alleles in the CHD subjects were: 0.826 for the E3, 0.137 for the E4 and 0.0362 for the E2. These frequencies are comparable to those found in the control group which were: 0.875 for the E3, 0.073 for the E4 and 0.0515 for the E2. No statistically significant differences in ApoE genotypes were found between the patients and the control groups. Moreover, there was no significant difference between the mean of triglyceride and HDL among the different ApoE genotypes. However, there was a significant difference in the mean of LDL and ApoE genotypes where the mean of LDL was (218.17mg\dl) in ApoE4, (149.67mg\dl) in ApoE2 and (184.52mg\dl) in ApoE3. A significant difference was also evident between the mean of LDL levels in the CHD and the control group where the mean of LDL was (126mg\dl) in CHD and (111.47mg\dl) in the control group. Our study indicated that there was no significant difference between the mean of cholesterol and triglyceride levels of the CHD and the control groups. To our knowledge, this is the first study in Gaza Strip investigating the relation between ApoE genotypes and CHD. Further investigations are needed to link other genetic factors to CHD.