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Flavin containing monooxygenase 3 genetic polymorphisms Glu158Lys and Glu308Gly and their relation to ischemic stroke

Aysun Türkanoğlu Özçelik1, Birsen Can Demirdöğen, Seref Demirkaya

  • 1Department of Biochemistry, Institute of Natural and Applied Sciences, Middle East Technical University, 06800 Ankara, Turkey. aysunturkanoglu@gmail.com

Gene
|March 21, 2013
PubMed

Insights

This study investigated FMO3 gene variants and ischemic stroke risk in the Turkish population. While no overall association was found, specific FMO3 genotypes increased stroke risk in hypertensive and obese individuals.

Area of Science:

  • Genetics
  • Neurology
  • Cardiovascular Disease

Background:

  • Ischemic stroke is a leading cause of death and disability, with poorly understood genetic underpinnings.
  • Oxidative stress from reactive oxygen species contributes to atherosclerosis, a major cause of ischemic stroke.
  • The FMO3 gene's role in ischemic stroke pathogenesis requires further investigation.

Purpose of the Study:

  • To examine the association between FMO3 gene variants (Glu158Lys and Glu308Gly) and ischemic stroke risk.
  • To analyze these associations within the Turkish population.
  • To explore potential gene-environment interactions with hypertension and obesity.

Main Methods:

  • Case-control study design involving 245 ischemic stroke cases and 145 controls.
  • Genotyping of two FMO3 single nucleotide polymorphisms (SNPs): Glu158Lys and Glu308Gly using PCR-RFLP.
  • Statistical analysis including case-control comparisons and subgroup analyses for hypertension and obesity.

Main Results:

  • No significant overall association between FMO3 Glu158Lys/Glu308Gly polymorphisms and ischemic stroke risk.
  • Heterozygous FMO3 genotypes (158Glu/Lys and 308Glu/Gly) significantly increased stroke risk by approximately 6-fold in hypertensive subjects.
  • Wild-type FMO3 genotypes (158Glu/Glu and 308Glu/Glu) were associated with a 6.2-fold and 4.8-fold higher risk of ischemic stroke in obese individuals, respectively.

Conclusions:

  • FMO3 gene variants do not appear to be a general risk factor for ischemic stroke in the Turkish population.
  • Specific FMO3 genotypes demonstrate a significant gene-environment interaction, increasing ischemic stroke risk in conjunction with hypertension and obesity.
  • This study provides novel insights into the genetic susceptibility of ischemic stroke, particularly in relation to metabolic factors in the Turkish population.

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