Source:http://linkedlifedata.com/resource/pubmed/id/10844412
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2000-7-24
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| pubmed:abstractText |
We investigated the relationship of codon 972 polymorphism of the insulin receptor substrate-1 (IRS-1) gene with insulin resistance in the Japanese population. Among 130 patients with type-2 diabetes mellitus (DM), we identified 6 who were heterozygous for the Gly972Arg mutation. Among 144 healthy subjects, 6 were heterozygous and 1 was homozygous for the mutation. A hyperinsulinemic euglycemic clamp study was performed in 3 of 6 diabetic patients with the heterozygous Gly972Arg mutation and in 60 without it. Both groups showed almost the same levels of insulin sensitivity (glucose infusion rate, GIR = 50.2 +/- 3.0 vs. 51.3 +/- 12.1 micromol/kg/min). Similarly, there was no difference in insulin sensitivity between healthy subjects with and without the mutation using the homeostasis model assessment (HOMA index = 1.14 +/- 0.50 vs. 1.02 +/- 0.63). The frequency of the Gly972Arg allele was not increased in diabetic patients compared with control subjects even in aged (>50 years old) or obese (BMI >/=25) subjects. Among healthy subjects, we identified a 25-year-old male with the homozygous Gly972Arg allele. He was slightly obese (BMI = 25.5) but showed relatively high insulin sensitivity, almost equal to that of healthy subjects without the mutation (GIR = 67.2 vs. 71.8 +/- 22.0 micromol/kg/min). Because the GIR in healthy subjects was significantly higher compared with that in type-2 DM patients, we speculate that another genetic or environmental factor producing a more deleterious effect on insulin sensitivity may exist in diabetic patients. We conclude that this gene abnormality does not play a role in the pathogenesis of insulin resistance and type-2 DM.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Codon,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/IRS1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin Receptor Substrate Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Insulin
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| pubmed:status |
MEDLINE
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| pubmed:issn |
0301-0163
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2000 S. Karger AG, Basel
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| pubmed:issnType |
Print
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| pubmed:volume |
52
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
230-4
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:10844412-Adult,
pubmed-meshheading:10844412-Aged,
pubmed-meshheading:10844412-Alleles,
pubmed-meshheading:10844412-Base Sequence,
pubmed-meshheading:10844412-Case-Control Studies,
pubmed-meshheading:10844412-Codon,
pubmed-meshheading:10844412-DNA Primers,
pubmed-meshheading:10844412-Diabetes Mellitus, Type 2,
pubmed-meshheading:10844412-Female,
pubmed-meshheading:10844412-Gene Frequency,
pubmed-meshheading:10844412-Heterozygote,
pubmed-meshheading:10844412-Homozygote,
pubmed-meshheading:10844412-Humans,
pubmed-meshheading:10844412-Insulin Receptor Substrate Proteins,
pubmed-meshheading:10844412-Insulin Resistance,
pubmed-meshheading:10844412-Male,
pubmed-meshheading:10844412-Middle Aged,
pubmed-meshheading:10844412-Phosphoproteins,
pubmed-meshheading:10844412-Point Mutation,
pubmed-meshheading:10844412-Polymorphism, Genetic,
pubmed-meshheading:10844412-Receptor, Insulin
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| pubmed:year |
1999
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| pubmed:articleTitle |
Insulin sensitivity is not affected by mutation of codon 972 of the human IRS-1 gene.
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| pubmed:affiliation |
Third Department of Internal Medicine, Mie University School of Medicine, Mie, Japan.
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| pubmed:publicationType |
Journal Article
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