ApoB plays a central role in lipoprotein metabolism through regulation of total cholesterol and LDL-cholesterol (LDL-C) concentrations in plasma. Two restriction fragment length polymorphisms (ECoRI and XbaI) represent single base alterations in the coding region of ApoB gene. ECoRI polymorphic region of ApoB gene is due to on an amino acid change (Glu→Lys). The XbaI polymorphic region of ApoB gene results from a substitution of (A→T) in the threonine codon and does not change the amino acid sequence.
In this study, we aimed the determine ECoRI and XbaI restriction enzyme polymorphisms of ApoB gene with respect to carotis intima media thickness (CIMT) in 238 type II diabetic patients and 118 control subjects. After polymerase chain reaction with specific primers for ApoB gene, PCR products were digested (ECoRI and XbaI), electrophoresed and visualized.
No significant changes in cholesterol, TG, HDL-C, LDL-C, Apo A and ApoB levels were determined between control and type II diabetic subjects. The frequencies of XbaI polymorphism in diabetic patients were 42.5% XX, 48.4% Xx and 9.1% xx; and in control subjects 44.4% XX, 44.4% Xx and 11.2% xx (P>0.05). The ECoRI frequencies are 2.2% EE, 41.1% Ee and 56.7% ee in diabetic patients; 7.8% EE, 23.7% Ee and 68.4% ee in controls (P<0.0442). CIMT measurements were significantly increased in diabetic subjects (P=0.0040).
Our results suggest that there was a relation between the ECoRI polymorphic site of ApoB gene with CIMT in type II diabetic patiens. It is possible that ECoRI polymorphic site of ApoB gene leads to oxidation of LDL-C and thereby an increase in CIMT.