| pubmed-article:21436039 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21436039 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
| pubmed-article:21436039 | lifeskim:mentions | umls-concept:C0031727 | lld:lifeskim |
| pubmed-article:21436039 | lifeskim:mentions | umls-concept:C0021655 | lld:lifeskim |
| pubmed-article:21436039 | lifeskim:mentions | umls-concept:C0456387 | lld:lifeskim |
| pubmed-article:21436039 | lifeskim:mentions | umls-concept:C0332206 | lld:lifeskim |
| pubmed-article:21436039 | pubmed:issue | 14 | lld:pubmed |
| pubmed-article:21436039 | pubmed:dateCreated | 2011-4-6 | lld:pubmed |
| pubmed-article:21436039 | pubmed:abstractText | Obesity and insulin resistance, the key features of metabolic syndrome, are closely associated with a state of chronic, low-grade inflammation characterized by abnormal macrophage infiltration into adipose tissues. Although it has been reported that chemokines promote leukocyte migration by activating class IB phosphoinositide-3 kinase (PI3K?) in inflammatory states, little is known about the role of PI3K? in obesity-induced macrophage infiltration into tissues, systemic inflammation, and the development of insulin resistance. In the present study, we used murine models of both diet-induced and genetically induced obesity to examine the role of PI3K? in the accumulation of tissue macrophages and the development of obesity-induced insulin resistance. Mice lacking p110? (Pik3cg(-/-)), the catalytic subunit of PI3K?, exhibited improved systemic insulin sensitivity with enhanced insulin signaling in the tissues of obese animals. In adipose tissues and livers of obese Pik3cg(-/-) mice, the numbers of infiltrated proinflammatory macrophages were markedly reduced, leading to suppression of inflammatory reactions in these tissues. Furthermore, bone marrow-specific deletion and pharmacological blockade of PI3K? also ameliorated obesity-induced macrophage infiltration and insulin resistance. These data suggest that PI3K? plays a crucial role in the development of both obesity-induced inflammation and systemic insulin resistance and that PI3K? can be a therapeutic target for type 2 diabetes. | lld:pubmed |
| pubmed-article:21436039 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21436039 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21436039 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:21436039 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21436039 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21436039 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21436039 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21436039 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21436039 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:21436039 | pubmed:issn | 1091-6490 | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:UekiKohjiroK | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:KobayashiNaok... | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:MurakamiKojiK | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:NagaiRyozoR | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:KadowakiTakas... | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:KubotaNaotoN | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:YoshimuraKota... | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:HaraKazuoK | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:KobayashiMasa... | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:SasakiTakehik... | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:SasakiJunkoJ | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:KurokawaMineo... | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:KoshimaIsaoI | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:KanekoKazumaK | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:OhsugiMitsuru... | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:SuzukiMihoM | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:GoyamaSusumuS | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:IwaneAyaA | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:OkazakiYukiko... | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:AwazawaMotoha... | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:SasakoTakayos... | lld:pubmed |
| pubmed-article:21436039 | pubmed:author | pubmed-author:NishikawaYosh... | lld:pubmed |
| pubmed-article:21436039 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21436039 | pubmed:day | 5 | lld:pubmed |
| pubmed-article:21436039 | pubmed:volume | 108 | lld:pubmed |
| pubmed-article:21436039 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21436039 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21436039 | pubmed:pagination | 5753-8 | lld:pubmed |
| pubmed-article:21436039 | pubmed:dateRevised | 2011-10-5 | lld:pubmed |
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| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
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| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
| pubmed-article:21436039 | pubmed:meshHeading | pubmed-meshheading:21436039... | lld:pubmed |
| pubmed-article:21436039 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21436039 | pubmed:articleTitle | Blockade of class IB phosphoinositide-3 kinase ameliorates obesity-induced inflammation and insulin resistance. | lld:pubmed |
| pubmed-article:21436039 | pubmed:affiliation | Department of Metabolic Diseases, Graduate School of Medicine, and Translational Systems Biology and Medicine Initiative, University of Tokyo, Tokyo 113-0033, Japan. | lld:pubmed |
| pubmed-article:21436039 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21436039 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:30955 | entrezgene:pubmed | pubmed-article:21436039 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:21436039 | lld:entrezgene |
