| pubmed-article:16150868 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16150868 | lifeskim:mentions | umls-concept:C0600251 | lld:lifeskim |
| pubmed-article:16150868 | lifeskim:mentions | umls-concept:C0206131 | lld:lifeskim |
| pubmed-article:16150868 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
| pubmed-article:16150868 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:16150868 | lifeskim:mentions | umls-concept:C0036720 | lld:lifeskim |
| pubmed-article:16150868 | lifeskim:mentions | umls-concept:C0123658 | lld:lifeskim |
| pubmed-article:16150868 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:16150868 | lifeskim:mentions | umls-concept:C1709915 | lld:lifeskim |
| pubmed-article:16150868 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:16150868 | pubmed:dateCreated | 2005-12-28 | lld:pubmed |
| pubmed-article:16150868 | pubmed:abstractText | Proinflammatory cytokines are recently reported to inhibit insulin signaling causing insulin resistance. IL-1alpha is also one of the proinflammatory cytokines; however, it has not been clarified whether IL-1alpha may also cause insulin resistance. Here, we investigated the effects of IL-1alpha treatment on insulin signaling in 3T3-L1 adipocytes. IL-1alpha treatment up to 4 h did not alter insulin-stimulated insulin receptor tyrosine phosphorylation, whereas tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and the association with phosphatidylinositol 3-kinase were partially inhibited with the maximal inhibition in around 15 min. IRS-1 was transiently phosphorylated on some serine residues around 15 min after IL-1alpha stimulation, when several serine kinases, IkappaB kinase, c-Jun-N-terminal kinase, ERK, and p70S6K were activated. Chemical inhibitors for these kinases inhibited IL-1alpha-induced serine phosphorylation of IRS-1. Tyrosine phosphorylation of IRS-1 was recovered only by the IKK inhibitor or JNK inhibitor, suggesting specific involvement of these two kinases. Insulin-stimulated Akt phosphorylation and 2-deoxyglucose uptake were not inhibited only by IL-1alpha. Interestingly, Akt phosphorylation was synergistically inhibited by IL-1alpha in the presence of IL-6. Taken together, short-term IL-1alpha treatment transiently causes insulin resistance at IRS-1 level with its serine phosphorylation. IL-1alpha may suppress insulin signaling downstream of IRS-1 in the presence of other cytokines, such as IL-6. | lld:pubmed |
| pubmed-article:16150868 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16150868 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16150868 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16150868 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:16150868 | pubmed:issn | 0888-8809 | lld:pubmed |
| pubmed-article:16150868 | pubmed:author | pubmed-author:KobayashiMasa... | lld:pubmed |
| pubmed-article:16150868 | pubmed:author | pubmed-author:UsuiIsaoI | lld:pubmed |
| pubmed-article:16150868 | pubmed:author | pubmed-author:SasaokaToshiy... | lld:pubmed |
| pubmed-article:16150868 | pubmed:author | pubmed-author:HarutaTetsuro... | lld:pubmed |
| pubmed-article:16150868 | pubmed:author | pubmed-author:IwataMinoruM | lld:pubmed |
| pubmed-article:16150868 | pubmed:author | pubmed-author:HirataniKazuy... | lld:pubmed |
| pubmed-article:16150868 | pubmed:author | pubmed-author:HeJianyingJ | lld:pubmed |
| pubmed-article:16150868 | pubmed:author | pubmed-author:IshizukaKenK | lld:pubmed |
| pubmed-article:16150868 | pubmed:author | pubmed-author:KanataniYukik... | lld:pubmed |
| pubmed-article:16150868 | pubmed:author | pubmed-author:BukhariAgussa... | lld:pubmed |
| pubmed-article:16150868 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16150868 | pubmed:volume | 20 | lld:pubmed |
| pubmed-article:16150868 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16150868 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16150868 | pubmed:pagination | 114-24 | lld:pubmed |
| pubmed-article:16150868 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
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| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
| pubmed-article:16150868 | pubmed:meshHeading | pubmed-meshheading:16150868... | lld:pubmed |
| pubmed-article:16150868 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16150868 | pubmed:articleTitle | Interleukin-1alpha inhibits insulin signaling with phosphorylating insulin receptor substrate-1 on serine residues in 3T3-L1 adipocytes. | lld:pubmed |
| pubmed-article:16150868 | pubmed:affiliation | The First Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama 930-0194, Japan. | lld:pubmed |
| pubmed-article:16150868 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16150868 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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