Comparison of Lipid Profiles with AP0A1 MspI Polymorphism in Obese Children with Hyperlipidemia

Abstract

Background: Obesity is a multifactorial, chronic disorder leading. to adverse metabolic effects on plasma lipid levels. Apolipoprotein AI (Apo AI) is the major structural component of high-density lipoprotein (HDL) and is involved in the esterification of cholesterol as a cofactor of lecithin-cholesterol acyltransferase (LCAT) and thus plays a major role in cholesterol efflux from peripheral cells. The APOA1 gene is associated with changes in lipid metabolism. A common gene polymorphism described in the APOA1 promoter region consists of the exchange of guanine (G) for adenine (A) at a position -75 bp upstream of the transcription origin. The relationship between lipid levels in obese children and the APOA1 MspI polymorphisms, was examined. Materials and Methods: Three separate groups were included, the patient group of obese children with hyperlipidemia; the obese control group (control group I) consisted of obese children without hyperlipidemia: and the healthy control group (control group II) contained healthy children with neither hyperlipidemia nor obesity. The related gene segments were amplified by polymerase chain reaction and determined different patterns were determined using denaturating gradient gel electrophoresis and positive results were confirmed automatic sequence analysis. All the results were analyzed by Proseq and BioEdit computer programmes. Results: The A allele was found to be more frequent in control group I compared to the patient group (p=0.035). Very low-density lipoprotein (VLDL), LDL and triglyceride (TG), levels were statistically higher in the patients carrying the GA genotype than in control group I. and body mass index (BMI), VLDL and TG levels were statistically higher than in control group II (p0.05). Additionally, according to the -75 GA genotypes, those in control group I with the GA genotype had elevated total cholesterol levels compared to those with the GG genotype (p<0.010). In conclusion, carrying the A. allele could confer a higher risk of hyperlipidemia in obese children.