title: Apolipoprotein A5 IVS3+476A allelic variant associates with increased trigliceride levels and confers risk for development of metabolic syndrome in Hungarians.
abstract: BACKGROUND
  Metabolic syndrome consists of multiple risk factors that are increasing the cardiovascular mortality. The T-1131C variant of the apolipoprotein A5 gene, associated with increased triglycerides, has been found to confer risk for cardiovascular diseases and metabolic syndrome. Because other naturally occurring variants of the gene also correlate with elevated triglycerides, the possible role of 2 common variants, the IVS3+G476A and T1259C, with metabolic syndrome was investigated.
  
  
  RESULTS
  A total of 213 metabolic syndrome patients and 142 healthy controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism. Serum triglycerides were increased in carriers compared with non-carriers in both groups (p<0.001); serum cholesterol levels were similar in all genotypes. The IVS3+476A allele frequency was increased in metabolic syndrome patients compared with controls (8.05 vs 2.47%; p<0.05), whereas the 1259C allele frequency did not differ between the groups. Multiple logistic regression analyses adjusted for age, gender, serum total cholesterol, acute myocardial infarction and stroke revealed that the IVS3+476A variant confers risk for development of metabolic syndrome (odds ratio =3.529, 95% confidence interval 1.308-9.029, p=0.009), but the 1259C allele had no such an effect.
  
  
  CONCLUSIONS
  Carrying the IVS3+473A allele is associated with elevated triglycerides and confers risk for development of metabolic syndrome, a combination that represents increased risk for development of atherogenic vascular diseases.
authors.affiliation: Department of Medical Genetics and Child Development, University of Pécs, Pécs, Hungary.
authors.forename: Péter
authors.initials: P
authors.lastname: Kisfali
authors.forename: Márton
authors.initials: M
authors.lastname: Mohás
authors.forename: Anita
authors.initials: A
authors.lastname: Maasz
authors.forename: Ferenc
authors.initials: F
authors.lastname: Hadarits
authors.forename: Lajos
authors.initials: L
authors.lastname: Markó
authors.forename: Katalin
authors.initials: K
authors.lastname: Horvatovich
authors.forename: Tamás
authors.initials: T
authors.lastname: Oroszlán
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Bagosi
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Bujtor
authors.forename: Beáta
authors.initials: B
authors.lastname: Gasztonyi
authors.forename: István
authors.initials: I
authors.lastname: Wittmann
authors.forename: Béla
authors.initials: B
authors.lastname: Melegh
mesh_terms: D000483:Alleles; D000072040:Apolipoprotein A-V; D001054:Apolipoproteins A / Q000235:genetics*; D050197:Atherosclerosis; D016022:Case-Control Studies; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D006814:Hungary / Q000453:epidemiology; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology / Q000235:genetics*; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012044:Regression Analysis; D012306:Risk; D014280:Triglycerides / Q000097:blood*
chemical_list: C437704:APOA5 protein, human; D000072040:Apolipoprotein A-V; D001054:Apolipoproteins A; D014280:Triglycerides