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内向整流钾通道6.2基因E23K多态性与2型糖尿病表型及格列齐特降糖疗效的关系 被引量:2

Association of E23K polymorphism of inwardly rectifying K^+channel 6.2 gene with the phenotype of type 2 diabetes and glucose-lowering effect of gliclazide
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摘要 研究内向整流钾通道6.2(Kir6.2)基因E23K多态性对2型糖尿病临床表型及格列齐特降糖疗效的影响。结果提示K/K纯合子患者的血肌酐水平高于其它基因型患者(P<0.01),E23K多态性不影响格列齐特的降糖疗效。 The influences of E23K polymorphism of inwardly rectifying K^+ channel 6.2 (Kir6.2) gene on the clinical phenotype of type 2 diabetes and glucose-lowering effect of gliclazide were investigated. The result showed that E23K polymorphism did not influence glucose-lowering effect of gliclazide, but serum creatinine level of patients with K/K genotype was higher than those of E/E and E/K genotypes (P 〈 0.01 ).
出处 《中华内分泌代谢杂志》 CAS CSCD 北大核心 2007年第2期158-159,共2页 Chinese Journal of Endocrinology and Metabolism
基金 黑龙江省卫生厅科研课题(2005-225)
关键词 钾通道 内向整流 多态性 单核苷酸 糖尿病 2型 格列齐特 Potassium channel, inwardly rectifying Polymorphism, single nucleotide Diabetes mellitus, type 2 Gliclazide
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  • 1Nielsen EM, Hansen L, Carstensen B, et al. The E23K variant of Kir6. 2 associates with impaired pest OGTT serum insulin response and increased risk of type 2 diabetes. Diabetes, 2003,52:573-577.
  • 2Schwanstecher C, Meyer U, Schwanstecher M. Kir6. 2 polymorphism predisposes to type 2 diabetes by inducing overactivity of pancreatic-cell ATP-sensitive K^+ channels. Diabetes, 2002,51:875-879.
  • 3Brochiero E, Wallendorf B, Gagnon D, et al. Cloning of rabbit Kir6.1, SUR2A, and SUR2B: possible candidates for a renal KATP channel. Am J Physiol Renal Physiol, 2002,282 : F289-F300.
  • 4Evans WE, Mcleod HL. Pharmacogenomics-drug disposition, drug targets, and drag side effects. N Engl J Med, 2003,348:538-549.
  • 5Dorschner H, Brekardin E, Uhde I, et al. Stoichiometry of sulfonylureainduced ATP-sensitive potassium channel closure. Mol Pharmacol, 1999,55 : 1060 -1066.

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