| pubmed-article:18445780 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18445780 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
| pubmed-article:18445780 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:18445780 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
| pubmed-article:18445780 | lifeskim:mentions | umls-concept:C0031621 | lld:lifeskim |
| pubmed-article:18445780 | lifeskim:mentions | umls-concept:C0031727 | lld:lifeskim |
| pubmed-article:18445780 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:18445780 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:18445780 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:18445780 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:18445780 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18445780 | pubmed:dateCreated | 2008-6-19 | lld:pubmed |
| pubmed-article:18445780 | pubmed:abstractText | Insulin is used to control pro-inflammatory hyperglycemia in critically ill patients. However, recent studies suggest that insulin-induced hypoglycemia may negate its beneficial effects in these patients. It is noteworthy that recent evidence indicates that insulin has anti-inflammatory effects that are independent of controlling hyperglycemia. To date, the mechanism by which insulin directly reduces inflammation has not been elucidated. It is well established that insulin activates phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling in many cell types. We and others have shown that this pathway negatively regulates LPS-induced signaling and pro-inflammatory cytokine production in monocytic cells. We hypothesized that insulin inhibits inflammation during endotoxemia by activation of the PI3K/Akt pathway. We used a nonhyperglycemic mouse model of endotoxemia to determine the effect of continuous administration of a low dose of human insulin on inflammation and survival. It is noteworthy that insulin treatment induced phosphorylation of Akt in muscle and adipose tissues but did not exacerbate lipopolysaccharide (LPS)-induced hypoglycemia. Insulin decreased plasma levels of interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein 1 (MCP1)/JE, and keratinocyte chemoattractant, and decreased mortality. The PI3K inhibitor wortmannin abolished the insulin-mediated activation of Akt and the reduction of chemokine and interleukin-6 levels. We conclude that insulin reduces LPS-induced inflammation in mice in a PI3K/Akt-dependent manner without affecting blood glucose levels. | lld:pubmed |
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| pubmed-article:18445780 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18445780 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18445780 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18445780 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18445780 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:18445780 | pubmed:issn | 1521-0103 | lld:pubmed |
| pubmed-article:18445780 | pubmed:author | pubmed-author:MackmanNigelN | lld:pubmed |
| pubmed-article:18445780 | pubmed:author | pubmed-author:LuyendykJames... | lld:pubmed |
| pubmed-article:18445780 | pubmed:author | pubmed-author:TilleyRachel... | lld:pubmed |
| pubmed-article:18445780 | pubmed:author | pubmed-author:HolscherTodd... | lld:pubmed |
| pubmed-article:18445780 | pubmed:author | pubmed-author:TencatiMichae... | lld:pubmed |
| pubmed-article:18445780 | pubmed:author | pubmed-author:KiddLinda BLB | lld:pubmed |
| pubmed-article:18445780 | pubmed:author | pubmed-author:SchabbauerGer... | lld:pubmed |
| pubmed-article:18445780 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18445780 | pubmed:volume | 326 | lld:pubmed |
| pubmed-article:18445780 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18445780 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18445780 | pubmed:pagination | 348-53 | lld:pubmed |
| pubmed-article:18445780 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:18445780 | pubmed:meshHeading | pubmed-meshheading:18445780... | lld:pubmed |
| pubmed-article:18445780 | pubmed:meshHeading | pubmed-meshheading:18445780... | lld:pubmed |
| pubmed-article:18445780 | pubmed:meshHeading | pubmed-meshheading:18445780... | lld:pubmed |
| pubmed-article:18445780 | pubmed:meshHeading | pubmed-meshheading:18445780... | lld:pubmed |
| pubmed-article:18445780 | pubmed:meshHeading | pubmed-meshheading:18445780... | lld:pubmed |
| pubmed-article:18445780 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18445780 | pubmed:articleTitle | Insulin activation of the phosphatidylinositol 3-kinase/protein kinase B (Akt) pathway reduces lipopolysaccharide-induced inflammation in mice. | lld:pubmed |
| pubmed-article:18445780 | pubmed:affiliation | The Department of Immunology, The Scripps Research Institute, La Jolla, California, USA. | lld:pubmed |
| pubmed-article:18445780 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18445780 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:18445780 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
