• Title/Summary/Keyword: IRS1 genetic polymorphism

Search Result 2, Processing Time 0.014 seconds

Overweight of Korean Male Workers and Genetic Polymorphism of Insulin Receptor Substrate 1 (IRS1) Gene

  • Kim, Ki-Woong;Heo, Kyung-Hwa;Won, Yong-Lim;Ko, Kyung-Sun;Kim, Tae-Gyun;Lee, Mi-Young;Park, Jung-Sun;Paik, Sang-Gi
    • Animal cells and systems
    • /
    • v.13 no.2
    • /
    • pp.127-132
    • /
    • 2009
  • We have examined the hypothesis that the Gly972Arg variant of the insulin receptor substrate 1 (IRS1) gene is associated with the components contributing to overweight (obesity) and metabolic syndrome. We describe IRS1 genotype frequencies in 274 Korean men. The frequencies of Gly972Gly (GIG) and Gly972Arg (G/A variant) of the IRS1 gene were 88.3% and 11.7%, respectively, and the differences in frequencies between the overweight (BMI$\geq$25kg/m$^2$) group and non-overweight (BMI<25kg/m$^2$) group were statistically significant. The subjects with G/A variant of IRS1 gene in non-overweight had significantly higher level of visceral fat thickness and adiponectin/leptin ratio than those with GIG alleles. In overweight group, the subjects with G/A variant of IRS1 gene also showed significantly higher level of insulin than those with GIG alleles. These results suggest that the IRS1 genetic polymorphism is involved in the occurrence of overweight, as well as metabolic syndrome.

Association of Insulin Receptor Substrate-1 G972R Variant with Non-small Cell Lung Cancer Risk

  • Lee, Chang Youl;Ahn, Chul Min;Jeon, Jeong Hee;Kim, Hyung Jung;Kim, Se Kyu;Chang, Joon;Kim, Sung Kyu;Chang, Yoon Soo
    • Tuberculosis and Respiratory Diseases
    • /
    • v.67 no.1
    • /
    • pp.8-13
    • /
    • 2009
  • Background: The insulin receptor substrate-1 (IRS-1) is the primary docking molecule for the insulin-like growth factor I receptor (IGF-IR), and is required for activation of the phosphatidylinositol 3'-kinase (PI3K) pathway. IRS-1 activation of the (PI3K) pathway regulates IGF-mediated survival, enhancement of cellular motility and apoptosis. Therefore, we attempted to ascertain whether IRS-1 genetic variations affect an individual's risk for non-small cell lung cancer (NSCLC). Methods: Two-hundred and eighteen subjects, either diagnosed with NSCLC or control subjects, were matched by age, gender and smoking status. Genomic DNA from each subject was amplified by PCR and analyzed according to the restriction fragment length polymorphism (RFLP) profile to detect the IRS-1 G972R polymorphism. Results: The frequencies of each polymorphic variation, in the control population, were as follows: GG=103 (94.5%) and GR=6 (5.5%); for the NSCLC subjects, the genotypic frequencies were as follows: GG=106 (97.2%) and GR=3 (2.8%). We could not demonstrate statistically significant differences in the genotypic distribution between the NSCLC and the control subjects (p=0.499, Fisher's Exact test). The relative risk of NSCLC, associated with the IRS-1 G972R polymorphic variation, was 1.028 (95% CI; 0.63~9.90). In addition, we found no differences between polymorphic variants with regard to the histological subtype of NSCLC. Conclusion: We did not observe any noteworthy differences in the frequency of the IRS-1 G972R polymorphism in NSCLC patients, compared to control subjects. These results suggest suggesting that, in our study population, the IRS-1 G972R polymorphism does may not appear to be associated with an increased risk of NSCLC.