ArticleDiabetologia1996
Molecular scanning of the insulin receptor substrate-1 (IRS-1) gene in Japanese patients with NIDDM: identification of five novel polymorphisms.
Article in Diabetologia, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.
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Who cites it
14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.
- Pooled it
- Gly972Arg variant in the insulin receptor substrate-1 gene and association with Type 2 diabetes: a meta-analysis of 27 studies.Diabetologia · 2003Pooled it
- Diabetes mellitus with severe insulin resistance in a young male patient with a heterozygous pathogenicClinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2024Article
- Prevalence of Insulin Receptor Substrate-1 Gene (G972R) Polymorphism, Insulin Resistance, and Determination of β-Cell Function among Overweight and Obese Persons with Type 2 Diabetes Mellitus.Journal of the ASEAN Federation of Endocrine Societies · 2021Article
- Novel insulin receptor substrate 1 and 2 variants in breast and colorectal cancer.Oncology reports · 2013Article
- A novel spontaneous mutation of Irs1 in mice results in hyperinsulinemia, reduced growth, low bone mass and impaired adipogenesis.The Journal of endocrinology · 2010Article
- Influence of socioeconomic lifestyle factors and genetic polymorphism on type 2 diabetes occurrences among Tunisian Arab and Berber groups of Djerba Island.Pharmacogenomics and personalized medicine · 2009Article
- An association between a common variant (G972R) in the IRS-1 gene and sex hormone levels in post-menopausal breast cancer survivors.Breast cancer research and treatment · 2006Article
- Control of glycaemia: from molecules to men. Minkowski Lecture 2003.Diabetologia · 2004Review
- Candidate genes for type 2 diabetes.Reviews in endocrine & metabolic disorders · 2004 · on this mapReview
- Genetics of insulin resistance.Current diabetes reports · 2002Review
- The Gly972-->Arg amino acid polymorphism in IRS-1 impairs insulin secretion in pancreatic beta cells.The Journal of clinical investigation · 1999Article
- Protein-protein interaction in insulin signaling and the molecular mechanisms of insulin resistance.The Journal of clinical investigation · 1999Review
- ASSOCIATION OF IRS1 GLY971ARG GENE POLYMORPHISM WITH INSULIN RESISTANCE IN IRANIAN NEWLY DIAGNOSED DIABETIC ADULTS.Acta endocrinologica (Bucharest, Romania : 2005)Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Since the insulin receptor substrate-1 (IRS-1) is the major substrate of the insulin receptor tyrosine kinase and has been shown to activate phosphatidylinositol (PI) 3-kinase and promote GLUT4 translocation, the IRS-1 gene is a potential candidate for development of non-insulin-dependent diabetes mellitus (NIDDM). In this study, we have identified IRS-1 gene polymorphisms, evaluated their frequencies in Japanese subjects, and analysed the contribution of these polymorphisms to the development of NIDDM. The entire coding region of the IRS-1 gene of 94 subjects (47 NIDDM and 47 control subjects) was screened by polymerase chain reaction-single stranded conformation polymorphism (PCR-SSCP) analysis. Seven SSCP polymorphisms were identified. These corresponded to two previously identified polymorphisms [Gly971 --> Arg (GGG --> AGG) and Ala804 (GCA --> GCG)] as well as five novel polymorphisms [Pro190 --> Arg (CCC --> CGC), Met209 --> Thr (ATG --> ACG), Ser809 --> Phe (TCT --> TTT), Leu142 (CTT --> CTC), and Gly625 (GGC --> GGT)]. Although the prevalence of each of these polymorphisms was not statistically different between NIDDM and control subjects, the prevalence of the four IRS-1 polymorphisms with an amino acid substitution together was significantly higher in NIDDM than in control subjects (23.4 vs 8.5%, p < 0.05), and two substitutions (Met 209 --> Thr and Ser809 --> Phe) were found only in NIDDM patients. Equilibrium glucose infusion rates during a euglycaemic clamp in NIDDM and control subjects with the IRS-1 polymorphisms decreased by 29.5 and 22.0%, respectively on the average when compared to those in comparable groups without polymorphisms, although they were not statistically significant. Thus, IRS-1 polymorphisms may contribute in part to the insulin resistance and development of NIDDM in Japanese subjects; however, they do not account for the major part of the decrease in insulin-stimulated glucose uptake which is observed in subjects with clinically apparent NIDDM.
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