| pubmed-article:12176670 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12176670 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:12176670 | lifeskim:mentions | umls-concept:C0011860 | lld:lifeskim |
| pubmed-article:12176670 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:12176670 | lifeskim:mentions | umls-concept:C0019425 | lld:lifeskim |
| pubmed-article:12176670 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:12176670 | lifeskim:mentions | umls-concept:C0021655 | lld:lifeskim |
| pubmed-article:12176670 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:12176670 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:12176670 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12176670 | pubmed:dateCreated | 2002-8-14 | lld:pubmed |
| pubmed-article:12176670 | pubmed:abstractText | Insulin receptor substrate 1 (IRS-1) gene polymorphisms have been identified in type 2 diabetic patients; however, it is unclear how such polymorphisms contribute to the development of diabetes. Here we introduced obesity in heterozygous IRS-1 knockout (IRS-1(+/-)) mice by gold-thioglucose (GTG) injection and studied the impact of reduced IRS-1 expression on obesity-linked insulin resistance. GTG injection resulted in approximately 30% weight gain in IRS-1(+/-) and wild type (WT) mice, compared with saline-injected controls. There was no difference in insulin sensitivity between lean IRS-1(+/-) and lean WT. Elevated fasting insulin levels but no change in fasting glucose were noted in obese IRS-1(+/-) and WT compared with the respective lean controls. Importantly, fasting insulin in obese IRS-1(+/-) was 1.5-fold higher (P<0.05) than in obese WT, and an insulin tolerance test showed a profound insulin resistance in obese IRS-1(+/-) compared with obese WT. The islets of obese IRS-1(+/-) were 1.4-fold larger than those of obese WT. The expression of insulin receptor and IRS-1 and IRS-2 was decreased in obese IRS-1(+/-), which could in part explain the profound insulin resistance in these mice. Our results suggest that IRS-1 is the suspected gene for type 2 diabetes and its polymorphisms could worsen insulin resistance in the presence of other additional factors, such as obesity. | lld:pubmed |
| pubmed-article:12176670 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12176670 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12176670 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12176670 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12176670 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12176670 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12176670 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12176670 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12176670 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12176670 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12176670 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12176670 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12176670 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12176670 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:12176670 | pubmed:issn | 0022-0795 | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:YoshizatoKK | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:KahnC RCR | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:MatsumotoKK | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:HirashimaYY | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:ArakiEE | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:ShirotaniTT | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:ShirakamiAA | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:MiyamuraNN | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:ToyonagaTT | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:KawashimaJJ | lld:pubmed |
| pubmed-article:12176670 | pubmed:author | pubmed-author:TsuruzoeKK | lld:pubmed |
| pubmed-article:12176670 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12176670 | pubmed:volume | 174 | lld:pubmed |
| pubmed-article:12176670 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12176670 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12176670 | pubmed:pagination | 309-19 | lld:pubmed |
| pubmed-article:12176670 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:12176670 | pubmed:meshHeading | pubmed-meshheading:12176670... | lld:pubmed |
| pubmed-article:12176670 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12176670 | pubmed:articleTitle | Heterozygous knockout of the IRS-1 gene in mice enhances obesity-linked insulin resistance: a possible model for the development of type 2 diabetes. | lld:pubmed |
| pubmed-article:12176670 | pubmed:affiliation | Department of Metabolic Medicine, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto 860-8556, Japan. | lld:pubmed |
| pubmed-article:12176670 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12176670 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:12176670 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:16367 | entrezgene:pubmed | pubmed-article:12176670 | lld:entrezgene |
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