title: Apolipoprotein A5 gene promoter region T-1131C polymorphism associates with elevated circulating triglyceride levels and confers susceptibility for development of ischemic stroke.
abstract: The possible pathogenic role of triglycerides (TG) in the development of ischemic stroke is still under extensive investigation. Recently, apolipoprotein (apo)A5 gene promoter region T-1131C polymorphism has been shown to associate with elevated serum TG levels. In the current work, a total of 302 subjects were classified as being large vessel-associated, small vessel-associated, or belonging to a mixed group of ischemic stroke-affected patients. The level of TG was increased in all groups (p < 0.01). The apoA5-1131C allele frequency was approximately twofold in all groups of stroke patients compared with the controls (5 vs 10-12%; p < 0.05); and the apoA5-1131C allele itself was also found to associate with increased TG levels in all groups. In a multivariate logistic regression analysis model adjusted for differences in age, gender, serum cholesterol, hypertension, presence of diabetes mellitus, smoking and drinking habits, and ischemic heart disease, a significantly increased risk of developing stroke disease was found in patients carrying the apoA5-1131C allele (p < 0.05; odds ratio OR = 2.1 [1.3-4.7]); this association was also proven for all subtypes of the stroke. The results presented here suggest that the apoA5-1131C allele is an independent risk factor for the development of stroke. Being that apoA5 gene is under the control of the peroxisome proliferator-activated receptor alpha, theoretically, the current observations also can have long-term therapeutic consequences.
authors.affiliation: Department of Medical Genetics and Child Development, University of Pécs, Pécs, Hungary.
authors.forename: Viktória
authors.initials: V
authors.lastname: Havasi
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Szolnoki
authors.forename: Gábor
authors.initials: G
authors.lastname: Talián
authors.forename: Judit
authors.initials: J
authors.lastname: Bene
authors.forename: Katalin
authors.initials: K
authors.lastname: Komlósi
authors.forename: Anita
authors.initials: A
authors.lastname: Maász
authors.forename: Ferenc
authors.initials: F
authors.lastname: Somogyvári
authors.forename: András
authors.initials: A
authors.lastname: Kondacs
authors.forename: Mihály
authors.initials: M
authors.lastname: Szabó
authors.forename: Lajos
authors.initials: L
authors.lastname: Fodor
authors.forename: Anita
authors.initials: A
authors.lastname: Bodor
authors.forename: Béla
authors.initials: B
authors.lastname: Melegh
mesh_terms: D000328:Adult; D000368:Aged; D000072040:Apolipoprotein A-V; D001054:Apolipoproteins A / Q000235:genetics*; D002545:Brain Ischemia / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008019:Life Style; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D012307:Risk Factors; D020521:Stroke / Q000235:genetics*; D014280:Triglycerides / Q000097:blood*
chemical_list: C437704:APOA5 protein, human; D000072040:Apolipoprotein A-V; D001054:Apolipoproteins A; D014280:Triglycerides