Relationship between the Mutation of IRS-1 Gene and β3-adrenergic Receptor Gene
丁国宪
沈捷
陈家伟
1.Department of Endocrinology,the First Affiliated Hospital of Nanjing Medical University,2.Department of Endocrinology,the First Affiliated Hospital of Nanjing Medical University,3.Department of Endocrinology,the First Affiliated Hospital of Nanjing Medical University,
摘要:Objective To explore the relationship between the mutation of Insulin receptor substrate-1 ( IRS-1) gene and β3-adrenergic receptor (β3-AR) gene associated with insulin resistance, to further elucidate the etiology and pathogenesis of type 2 DM, hypertension and coronary heart disease. Methods 281 Chinese subjects are divided into three groups according to the oral glucose tolerance test (OGTT), The subjects were genotyped for the codon 64 of β3-AR gene, the codon 972 of IRS-1 gene polymorphisms by applying polymerase chain reaction (PCR) restriction fragment-length polymorphisms (RFLP) screening. Results Our study found that there was significantly increased frequency of IRS-1 gene mutation in IGT subjects and type 2 DM patients (P<0.05, 0.01, respectively), increased frequency of β3-AR gene mutation in type 2 DM patients (P<0.01), compared with NGT subjects. After adjusted for age, sex and plasma glucose, the level of insulin was significantly correlated with polymorphism of IRS-1 gene and β3-AR gene (P<0.001 in all ) by multiple regression analysis. In the models of Logistic regression, type 2 DM is closely related to age and family history (OR=3.1966, 1.4670; P=0.0272, 0.009; respectively), and to the polymorphism of β3-AR gene (OR=1.7380, P=0.0356), but not related to the polymorphism of IRS-1 gene. Conclusions These results suggest that mutation of IRS-1 gene may be the risk factor for insulin resistance, whereas mutation of β3-AR gene may be a common risk factor for insulin resistance, obesity, type 2 DM and hypertension.
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分类号:R3(基础医学)
论文发表日期:2001-07-02
在线出版日期:2025-08-15(本平台首次上网日期,不代表文献的发表时间)
页数:7( 84-90 )
南京医科大学学报(英文版)

南京医科大学学报(英文版)

CSCD
ISSN:1674-8301
年,卷(期):2001,15(2)