Functional variants of glucokinase regulatory protein and apolipoprotein A5 genes in ischemic stroke

L. Járomi, V. Csöngei, Noémi Polgár, Z. Szolnoki, A. Maász, Katalin Horvatovich, Bernadett Faragó, C. Sipeky, E. Sáfrány, L. Magyari, P. Kisfali, M. Mohás, Ingrid Janicsek, Lilla Lakner, B. Melegh

Research output: Article

19 Citations (Scopus)

Abstract

Both the natural variants of the apolipoprotein A5 (APOA5) and the glucokinase regulatory protein gene (GCKR) have been shown to associate with increased fasting triglyceride levels. Here, we investigated the possible association of the functional variants of these two genes with non-fasting triglyceride levels and their susceptibility nature in ischemic stroke. A total of 513 stroke patients and 172 healthy controls were genotyped. All the APOA5 variants (T-1131C, IVS3+G476A, C56G, and T1259C) were associated with increased triglyceride levels in all stroke patients and controls; except for T1259C, they all conferred risk for the disease. No such association was found for the examined GCKR rs1260326 (C1337T) variant. Furthermore, we examined the effects of specific combinations of the GCKR rs1260326 and APOA5 polymorphisms. Our findings confirmed the previous results regarding the association of APOA5 variants with triglyceride-level increase and stroke susceptibility of these alleles. By contrast, we could not detect any association of the studied GCKR allele with triglyceride levels or with the susceptibility of stroke in the same cohort of patients. In addition, the effect of APOA5 did not change significantly when specific combinations of the two genes were present.

Original languageEnglish
Pages (from-to)121-128
Number of pages8
JournalJournal of Molecular Neuroscience
Volume41
Issue number1
DOIs
Publication statusPublished - máj. 2010

Fingerprint

Apolipoproteins
Regulator Genes
Triglycerides
Stroke
Genes
Alleles
Fasting
glucokinase regulatory protein
Apolipoprotein A-V

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this

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title = "Functional variants of glucokinase regulatory protein and apolipoprotein A5 genes in ischemic stroke",
abstract = "Both the natural variants of the apolipoprotein A5 (APOA5) and the glucokinase regulatory protein gene (GCKR) have been shown to associate with increased fasting triglyceride levels. Here, we investigated the possible association of the functional variants of these two genes with non-fasting triglyceride levels and their susceptibility nature in ischemic stroke. A total of 513 stroke patients and 172 healthy controls were genotyped. All the APOA5 variants (T-1131C, IVS3+G476A, C56G, and T1259C) were associated with increased triglyceride levels in all stroke patients and controls; except for T1259C, they all conferred risk for the disease. No such association was found for the examined GCKR rs1260326 (C1337T) variant. Furthermore, we examined the effects of specific combinations of the GCKR rs1260326 and APOA5 polymorphisms. Our findings confirmed the previous results regarding the association of APOA5 variants with triglyceride-level increase and stroke susceptibility of these alleles. By contrast, we could not detect any association of the studied GCKR allele with triglyceride levels or with the susceptibility of stroke in the same cohort of patients. In addition, the effect of APOA5 did not change significantly when specific combinations of the two genes were present.",
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author = "L. J{\'a}romi and V. Cs{\"o}ngei and No{\'e}mi Polg{\'a}r and Z. Szolnoki and A. Ma{\'a}sz and Katalin Horvatovich and Bernadett Farag{\'o} and C. Sipeky and E. S{\'a}fr{\'a}ny and L. Magyari and P. Kisfali and M. Moh{\'a}s and Ingrid Janicsek and Lilla Lakner and B. Melegh",
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T1 - Functional variants of glucokinase regulatory protein and apolipoprotein A5 genes in ischemic stroke

AU - Járomi, L.

AU - Csöngei, V.

AU - Polgár, Noémi

AU - Szolnoki, Z.

AU - Maász, A.

AU - Horvatovich, Katalin

AU - Faragó, Bernadett

AU - Sipeky, C.

AU - Sáfrány, E.

AU - Magyari, L.

AU - Kisfali, P.

AU - Mohás, M.

AU - Janicsek, Ingrid

AU - Lakner, Lilla

AU - Melegh, B.

PY - 2010/5

Y1 - 2010/5

N2 - Both the natural variants of the apolipoprotein A5 (APOA5) and the glucokinase regulatory protein gene (GCKR) have been shown to associate with increased fasting triglyceride levels. Here, we investigated the possible association of the functional variants of these two genes with non-fasting triglyceride levels and their susceptibility nature in ischemic stroke. A total of 513 stroke patients and 172 healthy controls were genotyped. All the APOA5 variants (T-1131C, IVS3+G476A, C56G, and T1259C) were associated with increased triglyceride levels in all stroke patients and controls; except for T1259C, they all conferred risk for the disease. No such association was found for the examined GCKR rs1260326 (C1337T) variant. Furthermore, we examined the effects of specific combinations of the GCKR rs1260326 and APOA5 polymorphisms. Our findings confirmed the previous results regarding the association of APOA5 variants with triglyceride-level increase and stroke susceptibility of these alleles. By contrast, we could not detect any association of the studied GCKR allele with triglyceride levels or with the susceptibility of stroke in the same cohort of patients. In addition, the effect of APOA5 did not change significantly when specific combinations of the two genes were present.

AB - Both the natural variants of the apolipoprotein A5 (APOA5) and the glucokinase regulatory protein gene (GCKR) have been shown to associate with increased fasting triglyceride levels. Here, we investigated the possible association of the functional variants of these two genes with non-fasting triglyceride levels and their susceptibility nature in ischemic stroke. A total of 513 stroke patients and 172 healthy controls were genotyped. All the APOA5 variants (T-1131C, IVS3+G476A, C56G, and T1259C) were associated with increased triglyceride levels in all stroke patients and controls; except for T1259C, they all conferred risk for the disease. No such association was found for the examined GCKR rs1260326 (C1337T) variant. Furthermore, we examined the effects of specific combinations of the GCKR rs1260326 and APOA5 polymorphisms. Our findings confirmed the previous results regarding the association of APOA5 variants with triglyceride-level increase and stroke susceptibility of these alleles. By contrast, we could not detect any association of the studied GCKR allele with triglyceride levels or with the susceptibility of stroke in the same cohort of patients. In addition, the effect of APOA5 did not change significantly when specific combinations of the two genes were present.

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