| pubmed-article:16306364 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C0044602 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C0242692 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C1708272 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C0017725 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C0221099 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C0243067 | lld:lifeskim |
| pubmed-article:16306364 | lifeskim:mentions | umls-concept:C1707797 | lld:lifeskim |
| pubmed-article:16306364 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:16306364 | pubmed:dateCreated | 2005-11-24 | lld:pubmed |
| pubmed-article:16306364 | pubmed:abstractText | More than 40% of HIV-infected patients on highly active antiretroviral therapy (HAART) experience fat redistribution (lipodystrophy), a syndrome associated with insulin resistance primarily affecting insulin-stimulated nonoxidative glucose metabolism (NOGM(ins)). Skeletal muscle biopsies, obtained from 18 lipodystrophic nondiabetic patients (LIPO) and 18 nondiabetic patients without lipodystrophy (NONLIPO) before and during hyperinsulinemic (40 mU.m(-2).min(-1))-euglycemic clamps, were analyzed for insulin signaling effectors. All patients were on HAART. Both LIPO and NONLIPO patients were normoglycemic (4.9 +/- 0.1 and 4.8 +/- 0.1 mmol/l, respectively); however, NOGM(ins) was reduced by 49% in LIPO patients (P < 0.001). NOGM(ins) correlated positively with insulin-stimulated glycogen synthase activity (I-form, P < 0.001, n = 36). Glycogen synthase activity (I-form) correlated inversely with phosphorylation of glycogen synthase sites 2+2a (P < 0.001, n = 36) and sites 3a+b (P < 0.001, n = 36) during clamp. Incremental glycogen synthase-kinase-3alpha and -3beta phosphorylation was attenuated in LIPO patients (Ps < 0.05). Insulin-stimulated Akt Ser473 and Akt Thr308 phosphorylation was decreased in LIPO patients (P < 0.05), whereas insulin receptor substrate-1-associated phosphatidylinositol (PI) 3-kinase activity increased significantly (P < 0.001) and similarly (NS) in both groups during clamp. Thus, low glycogen synthase activity explained impaired NOGM(ins) in HIV lipodystrophy, and insulin signaling defects were downstream of PI 3-kinase at the level of Akt. These results suggest mechanisms for the insulin resistance greatly enhancing the risk of type 2 diabetes in HIV lipodystrophy. | lld:pubmed |
| pubmed-article:16306364 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16306364 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16306364 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16306364 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16306364 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16306364 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:16306364 | pubmed:issn | 0012-1797 | lld:pubmed |
| pubmed-article:16306364 | pubmed:author | pubmed-author:WojtaszewskiJ... | lld:pubmed |
| pubmed-article:16306364 | pubmed:author | pubmed-author:MadsbadStenS | lld:pubmed |
| pubmed-article:16306364 | pubmed:author | pubmed-author:AndersenOveO | lld:pubmed |
| pubmed-article:16306364 | pubmed:author | pubmed-author:HaugaardSteen... | lld:pubmed |
| pubmed-article:16306364 | pubmed:author | pubmed-author:NielsenJens... | lld:pubmed |
| pubmed-article:16306364 | pubmed:author | pubmed-author:IversenJohanJ | lld:pubmed |
| pubmed-article:16306364 | pubmed:author | pubmed-author:FrøsigChristi... | lld:pubmed |
| pubmed-article:16306364 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16306364 | pubmed:volume | 54 | lld:pubmed |
| pubmed-article:16306364 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16306364 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16306364 | pubmed:pagination | 3474-83 | lld:pubmed |
| pubmed-article:16306364 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:16306364 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16306364 | pubmed:articleTitle | Skeletal muscle insulin signaling defects downstream of phosphatidylinositol 3-kinase at the level of Akt are associated with impaired nonoxidative glucose disposal in HIV lipodystrophy. | lld:pubmed |
| pubmed-article:16306364 | pubmed:affiliation | Department of Infectious Diseases, Clinical Research Unit 136, Hvidovre University Hospital, DK 2650 Hvidovre, Copenhagen, Denmark. sbhau@dadlnet.dk | lld:pubmed |
| pubmed-article:16306364 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16306364 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16306364 | lld:pubmed |
