| pubmed-article:15824195 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15824195 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:15824195 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
| pubmed-article:15824195 | lifeskim:mentions | umls-concept:C0021655 | lld:lifeskim |
| pubmed-article:15824195 | lifeskim:mentions | umls-concept:C1704666 | lld:lifeskim |
| pubmed-article:15824195 | lifeskim:mentions | umls-concept:C1517892 | lld:lifeskim |
| pubmed-article:15824195 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:15824195 | lifeskim:mentions | umls-concept:C0208973 | lld:lifeskim |
| pubmed-article:15824195 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:15824195 | pubmed:dateCreated | 2005-4-29 | lld:pubmed |
| pubmed-article:15824195 | pubmed:abstractText | Insulin resistance is a major player in the pathogenesis of the metabolic syndrome and type 2 diabetes, and yet, the mechanisms responsible for it remain poorly understood. Magnetic resonance spectroscopy studies in humans suggest that a defect in insulin-stimulated glucose transport in skeletal muscle is the primary metabolic abnormality in insulin-resistant type 2 diabetics. Fatty acids appear to cause this defect in glucose transport by inhibiting insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1 associated phosphatidylinositol 3-kinase activity. A number of different metabolic abnormalities may increase intramyocellular/intrahepatic fatty acid metabolites; these include increased fat delivery to muscle/liver as a consequence of either excess energy intake or defects in adipocyte fat metabolism and acquired or inherited defects in mitochondrial fatty acid oxidation. Understanding the molecular/biochemical defects responsible for insulin resistance is beginning to unveil novel therapeutic targets for treatment of the metabolic syndrome and type 2 diabetes. | lld:pubmed |
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| pubmed-article:15824195 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15824195 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15824195 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15824195 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15824195 | pubmed:month | May | lld:pubmed |
| pubmed-article:15824195 | pubmed:issn | 1524-4563 | lld:pubmed |
| pubmed-article:15824195 | pubmed:author | pubmed-author:ShulmanGerald... | lld:pubmed |
| pubmed-article:15824195 | pubmed:author | pubmed-author:SavageDavid... | lld:pubmed |
| pubmed-article:15824195 | pubmed:author | pubmed-author:PetersenKitt... | lld:pubmed |
| pubmed-article:15824195 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:15824195 | pubmed:volume | 45 | lld:pubmed |
| pubmed-article:15824195 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15824195 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15824195 | pubmed:pagination | 828-33 | lld:pubmed |
| pubmed-article:15824195 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15824195 | pubmed:meshHeading | pubmed-meshheading:15824195... | lld:pubmed |
| pubmed-article:15824195 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15824195 | pubmed:articleTitle | Mechanisms of insulin resistance in humans and possible links with inflammation. | lld:pubmed |
| pubmed-article:15824195 | pubmed:affiliation | Department of Internal Medicine, Yale University School of Medicine, New Haven, Conn 06510, USA. | lld:pubmed |
| pubmed-article:15824195 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15824195 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15824195 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:15824195 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:15824195 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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