title: Comparison of lipid profiles with APOA1 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.
  
  
  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 (p<0.05). There was no relationship between -75(G/A) polymorphism and serum lipid HDL-cholesterol levels when patient values were compared to those of the controls (p>0.05). 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.
authors.affiliation: Department of Molecular Medicine, Institute of Experimental Medicine, Istanbul University, Capa-Istanbul, Turkey.
authors.forename: Bahar
authors.initials: B
authors.lastname: Toptas
authors.forename: Uzay
authors.initials: U
authors.lastname: Görmüş
authors.forename: Arzu
authors.initials: A
authors.lastname: Ergen
authors.forename: Hakan
authors.initials: H
authors.lastname: Gürkan
authors.forename: Fatih
authors.initials: F
authors.lastname: Keleşoglu
authors.forename: Feyza
authors.initials: F
authors.lastname: Darendeliler
authors.forename: Firdevs
authors.initials: F
authors.lastname: Bas
authors.forename: Altay Burak
authors.initials: AB
authors.lastname: Dalan
authors.forename: Güldal
authors.initials: G
authors.lastname: Izbirak
authors.forename: Turgay
authors.initials: T
authors.lastname: Isbir
mesh_terms: D000293:Adolescent; D000483:Alleles; D016632:Apolipoprotein A-I / Q000235:genetics*; D001483:Base Sequence; D002648:Child; D019003:Deoxyribonuclease HpaII / Q000378:metabolism; D005260:Female; D005787:Gene Frequency / Q000235:genetics; D005838:Genotype; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000150:complications / Q000235:genetics; D008055:Lipids / Q000097:blood*; D008297:Male; D008969:Molecular Sequence Data; D009765:Obesity / Q000097:blood / Q000150:complications / Q000235:genetics; D011110:Polymorphism, Genetic / Q000235:genetics*; D015995:Prevalence
chemical_list: D016632:Apolipoprotein A-I; D008055:Lipids; D019003:Deoxyribonuclease HpaII