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深圳汉族Kir6.2基因与2型糖尿病关系的病例-对照研究 被引量:1

Correlation of Membrane Glycoprotein Kir6.2 Gene Polymorphism with Type 2 Diabetes Mellitus and Insulin Resistance in Han Nationality in Shenzhen
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摘要 目的研究深圳汉族人群钾离子内向整流通道Kir6.2基因多态性与胰岛素抵抗(IR)特征和2型糖尿病(T2DM)的关系。方法运用聚合酶链反应-变性梯度凝胶电泳(PCR-DGGE)技术对深圳市251例T2DM患者和170例非DM对照(NGT)人群的Kir6.2基因第一外显子E23K多态性进行分析,并对T2DM组不同基因型间临床及生化指标进行比较。结果 T2DM组与非DM对照组比较,Kir6.2基因型频率和等位基因频率分布差别均无统计学意义;T2DM组携带K等位基因者空腹血糖(FPG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)及空腹血C肽(CP)水平显著高于携带E等位基因者(P<0.05)。结论深圳市汉族人群Kir6.2基因E23K多态性与2型DM患者胰岛素抵抗表型相关,但与T2DM的发生无明显关联。 Objective To explore the relationship of the E23K polymorphism of membrane glycoprotein Kit6.2 gene with the features of insulin resistance (IR) and type 2 diabetes mellitus (T2DM) in Han nationality of Shenzhen. Methods The E23K polymorphism in exon 1 of Kit6.2 gene were determined with the technique of polymerase chain reaction-denaturing gradient gel electrophoresis (PCR- DGGE) in 251 type 2 diabetic subjects and 170 normal glucose tolerance (NGT) control subjects in Shenzhen city. The clinical and laboratory data were also compared between type 2 diabetic patients with different genotypes. Results No statistically significant differences were observed in the genotype and allele frequencies between control subjects and type 2 diabetic subjects. The K allele was associated with higher fasting plasma glucose (FPG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and higher C-peptide (CP) concentrations than the E allele was in type 2 diabetic patients (P〈0.05). Conclusion The present study shows that the E23K polymorphism of Kir6.2 gene in Han nationality of Shenzhen is not associated with the occurrence of type 2 diabetes meihtas, but associated with insulin resistance in type 2 diabetic patients.
出处 《中国慢性病预防与控制》 CAS 北大核心 2011年第2期123-125,共3页 Chinese Journal of Prevention and Control of Chronic Diseases
关键词 KIR6.2基因 基因多态性 糖尿病 2型 胰岛素抵抗 Kir6.2 gene Gene polymorphism Diabetes mellitus, type 2 Insulin resistance
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  • 1Koster JC, Marshall BA, Ensor N, et al K-ATP channels induces profound 2000,100:645-654.
  • 2Targeted overactivity of beta cell neonatal diabetes[J]. Cell , Sakura H, Wat N, Horton V, et al. Sequence variations in the human Kir6.2 gene, a subunit of the beta-cell ATPsensitive K-channel: no association with NIDDM in white Caucasian subjects or evidence of abnormal function when expressed in vitro [ J ]. Diabetologia, 1996,39: 1233-1236.
  • 3Yamada Y, Kuroe A, Li Q, et al. Genomic variation in pancreatic ion channel genes in Japanese type 2 diabetic patients [J]. Diabetes- Metab Res Rev, 2001,17:213-216.
  • 4Inoue H, Ferrer J, Warren-Perry. M, et al. Sequence variants in the pancreatic islet B-cell inwardly rectifying K^+ channel Kit6.2 (Bir) genc: identification and lack of role in Caucasian patients with NIDDM [J].Diabetes. 1997.46: 502-507.
  • 5Altshuler D, Hirschhorn JN, Klannemark M, et al. The common PPAR gamma Prol2Ala polymorphism is associated with decreased risk of type 2 diabetes[J]. Nature Gene, 2000,26:76-80.
  • 6Hansen L, Echwald SM, Hansen T, et al. Amino acid polymorphisms in the ATP-regulatable inward rectifier Kir6.2 and their relationships to glucose-and tolbutamide-induced insulin secretion, the insulin sensitivity index, and NIDDM[J]. Diabetes, 1997,46:508-512.

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