| pubmed-article:11485987 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11485987 | lifeskim:mentions | umls-concept:C0011860 | lld:lifeskim |
| pubmed-article:11485987 | lifeskim:mentions | umls-concept:C0242692 | lld:lifeskim |
| pubmed-article:11485987 | lifeskim:mentions | umls-concept:C0015127 | lld:lifeskim |
| pubmed-article:11485987 | lifeskim:mentions | umls-concept:C0034818 | lld:lifeskim |
| pubmed-article:11485987 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
| pubmed-article:11485987 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
| pubmed-article:11485987 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
| pubmed-article:11485987 | pubmed:issue | 15 | lld:pubmed |
| pubmed-article:11485987 | pubmed:dateCreated | 2001-8-3 | lld:pubmed |
| pubmed-article:11485987 | pubmed:abstractText | Peripheral insulin resistance and impaired insulin action are the primary characteristics of type 2 diabetes. The first observable defect in this major disorder occurs in muscle, where glucose disposal in response to insulin is impaired. We have developed a transgenic mouse with a dominant-negative insulin-like growth factor-I receptor (KR-IGF-IR) specifically targeted to the skeletal muscle. Expression of KR-IGF-IR resulted in the formation of hybrid receptors between the mutant and the endogenous IGF-I and insulin receptors, thereby abrogating the normal function of these receptors and leading to insulin resistance. Pancreatic beta-cell dysfunction developed at a relative early age, resulting in diabetes. These mice provide an excellent model to study the molecular mechanisms underlying the development of human type 2 diabetes. | lld:pubmed |
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| pubmed-article:11485987 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11485987 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11485987 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11485987 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11485987 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:11485987 | pubmed:issn | 0890-9369 | lld:pubmed |
| pubmed-article:11485987 | pubmed:author | pubmed-author:DupontJJ | lld:pubmed |
| pubmed-article:11485987 | pubmed:author | pubmed-author:KimJ KJK | lld:pubmed |
| pubmed-article:11485987 | pubmed:author | pubmed-author:Le RoithDD | lld:pubmed |
| pubmed-article:11485987 | pubmed:author | pubmed-author:ShulmanG IGI | lld:pubmed |
| pubmed-article:11485987 | pubmed:author | pubmed-author:FernándezA... | lld:pubmed |
| pubmed-article:11485987 | pubmed:author | pubmed-author:YakarSS | lld:pubmed |
| pubmed-article:11485987 | pubmed:author | pubmed-author:CasaisCC | lld:pubmed |
| pubmed-article:11485987 | pubmed:author | pubmed-author:Hernandez-San... | lld:pubmed |
| pubmed-article:11485987 | pubmed:author | pubmed-author:FilmoreJJ | lld:pubmed |
| pubmed-article:11485987 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11485987 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11485987 | pubmed:volume | 15 | lld:pubmed |
| pubmed-article:11485987 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11485987 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11485987 | pubmed:pagination | 1926-34 | lld:pubmed |
| pubmed-article:11485987 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:11485987 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11485987 | pubmed:articleTitle | Functional inactivation of the IGF-I and insulin receptors in skeletal muscle causes type 2 diabetes. | lld:pubmed |
| pubmed-article:11485987 | pubmed:affiliation | Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health, Bethesda, Maryland 20892, USA. | lld:pubmed |
| pubmed-article:11485987 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11485987 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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