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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6670
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pubmed:dateCreated |
1998-3-19
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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.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/IRS1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IRS2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin Receptor Substrate Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Irs1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Irs2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
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:month |
Feb
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pubmed:issn |
0028-0836
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pubmed:author |
pubmed-author:BernalDD,
pubmed-author:Bonner-WeirSS,
pubmed-author:BurksD JDJ,
pubmed-author:GutierrezJ SJS,
pubmed-author:PonsSS,
pubmed-author:PrevinVV,
pubmed-author:RenJ MJM,
pubmed-author:ShulmanG IGI,
pubmed-author:TowertSS,
pubmed-author:WhiteM FMF,
pubmed-author:WithersD JDJ,
pubmed-author:ZhangYY
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pubmed:issnType |
Print
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pubmed:day |
26
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pubmed:volume |
391
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
900-4
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:9495343-Animals,
pubmed-meshheading:9495343-Blood Glucose,
pubmed-meshheading:9495343-Cloning, Molecular,
pubmed-meshheading:9495343-Diabetes Mellitus, Type 2,
pubmed-meshheading:9495343-Female,
pubmed-meshheading:9495343-Gene Targeting,
pubmed-meshheading:9495343-Humans,
pubmed-meshheading:9495343-Insulin,
pubmed-meshheading:9495343-Insulin Receptor Substrate Proteins,
pubmed-meshheading:9495343-Insulin Resistance,
pubmed-meshheading:9495343-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:9495343-Islets of Langerhans,
pubmed-meshheading:9495343-Liver,
pubmed-meshheading:9495343-Male,
pubmed-meshheading:9495343-Mice,
pubmed-meshheading:9495343-Mice, Inbred C57BL,
pubmed-meshheading:9495343-Muscle, Skeletal,
pubmed-meshheading:9495343-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:9495343-Phosphoproteins,
pubmed-meshheading:9495343-Phosphorylation,
pubmed-meshheading:9495343-Receptor, Insulin,
pubmed-meshheading:9495343-Recombination, Genetic,
pubmed-meshheading:9495343-Signal Transduction
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pubmed:year |
1998
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pubmed:articleTitle |
Disruption of IRS-2 causes type 2 diabetes in mice.
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pubmed:affiliation |
Howard Hughes Medical Institute, Joslin Diabetes Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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