| pubmed-article:9495343 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9495343 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:9495343 | lifeskim:mentions | umls-concept:C0011860 | lld:lifeskim |
| pubmed-article:9495343 | lifeskim:mentions | umls-concept:C0015127 | lld:lifeskim |
| pubmed-article:9495343 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
| pubmed-article:9495343 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
| pubmed-article:9495343 | pubmed:issue | 6670 | lld:pubmed |
| pubmed-article:9495343 | pubmed:dateCreated | 1998-3-19 | lld:pubmed |
| pubmed-article:9495343 | pubmed:abstractText | Human type 2 diabetes is characterized by defects in both insulin action and insulin secretion. It has been difficult to identify a single molecular abnormality underlying these features. Insulin-receptor substrates (IRS proteins) may be involved in type 2 diabetes: they mediate pleiotropic signals initiated by receptors for insulin and other cytokines. Disruption of IRS-1 in mice retards growth, but diabetes does not develop because insulin secretion increases to compensate for the mild resistance to insulin. Here we show that disruption of IRS-2 impairs both peripheral insulin signalling and pancreatic beta-cell function. IRS-2-deficient mice show progressive deterioration of glucose homeostasis because of insulin resistance in the liver and skeletal muscle and a lack of beta-cell compensation for this insulin resistance. Our results indicate that dysfunction of IRS-2 may contribute to the pathophysiology of human type 2 diabetes. | lld:pubmed |
| pubmed-article:9495343 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9495343 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9495343 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9495343 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:9495343 | pubmed:issn | 0028-0836 | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:PonsSS | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:Bonner-WeirSS | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:ShulmanG IGI | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:ZhangYY | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:BurksD JDJ | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:WhiteM FMF | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:BernalDD | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:RenJ MJM | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:WithersD JDJ | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:TowertSS | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:PrevinVV | lld:pubmed |
| pubmed-article:9495343 | pubmed:author | pubmed-author:GutierrezJ... | lld:pubmed |
| pubmed-article:9495343 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9495343 | pubmed:day | 26 | lld:pubmed |
| pubmed-article:9495343 | pubmed:volume | 391 | lld:pubmed |
| pubmed-article:9495343 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9495343 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9495343 | pubmed:pagination | 900-4 | lld:pubmed |
| pubmed-article:9495343 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:9495343 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9495343 | pubmed:articleTitle | Disruption of IRS-2 causes type 2 diabetes in mice. | lld:pubmed |
| pubmed-article:9495343 | pubmed:affiliation | Howard Hughes Medical Institute, Joslin Diabetes Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215, USA. | lld:pubmed |
| pubmed-article:9495343 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9495343 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9495343 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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