The E23K polymorphism in Kir6.2 gene and coronary heart disease

Clin Chim Acta. 2006 May;367(1-2):93-7. doi: 10.1016/j.cca.2005.11.032. Epub 2006 Feb 7.

Abstract

Background: The G to A mutation in the Kir 6.2, the ATP-sensitive potassium channel subunit, resulted a glutamate (E) to lysine (K) substitution at codon 23, and the A allele was shown to have a relationship with high risk to type 2 diabetes in previous study. Their role in coronary heart disease (CHD) has not been evaluated. We hypothesized that the polymorphism would be associated with increased susceptibility to CHD.

Methods: The E23K gene polymorphism of Kir6.2 gene was analyzed by PCR-restriction site polymorphism (PCR-RSP) methods in 101 controls and 119 CHD patients. Serum lipids and C reactive protein concentrations were measured in all subjects.

Results: Among the CHD patients, the frequency of the G allele was higher (63.4% vs. 56.9%, P>0.05) and the frequency of the A allele was lower (36.6% vs. 43.1%, P>0.05) than among controls. No significant differences were found in allele frequencies between CHD and controls (P>0.05), but there were significant differences in GG and combined (GA+AA) genotypes frequencies (42.0% vs. 28.7%, and 58.0% vs. 71.3%, P<0.050).

Conclusions: The E23K gene polymorphism in Kir6.2 gene appeared to be related to high susceptibility to CHD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • Blood Pressure
  • C-Reactive Protein / metabolism
  • Coronary Disease / genetics*
  • Coronary Disease / pathology
  • Female
  • Genotype
  • Glutamic Acid / genetics*
  • Humans
  • Lipid Metabolism
  • Male
  • Middle Aged
  • Polymorphism, Genetic / genetics*
  • Potassium Channels, Inwardly Rectifying / genetics*

Substances

  • Kir6.2 channel
  • Potassium Channels, Inwardly Rectifying
  • Glutamic Acid
  • C-Reactive Protein