| pubmed-article:9492058 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9492058 | lifeskim:mentions | umls-concept:C1720857 | lld:lifeskim |
| pubmed-article:9492058 | lifeskim:mentions | umls-concept:C0015127 | lld:lifeskim |
| pubmed-article:9492058 | lifeskim:mentions | umls-concept:C0521457 | lld:lifeskim |
| pubmed-article:9492058 | lifeskim:mentions | umls-concept:C0596843 | lld:lifeskim |
| pubmed-article:9492058 | lifeskim:mentions | umls-concept:C0034818 | lld:lifeskim |
| pubmed-article:9492058 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:9492058 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
| pubmed-article:9492058 | lifeskim:mentions | umls-concept:C0021655 | lld:lifeskim |
| pubmed-article:9492058 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:9492058 | pubmed:dateCreated | 1998-3-12 | lld:pubmed |
| pubmed-article:9492058 | pubmed:abstractText | Treatment of fetal brown adipocytes with 0.6 nM tumor necrosis factor (TNF)-alpha for 24 h resulted in a partial impairment in the expression of fatty acid synthase, glycerol-3-phosphate dehydrogenase, and glucose transporter (GLUT)-4 messenger RNAs (mRNAs), as well as in the enhancement in the cytoplasmic lipid content in response to insulin. However, the expression of the tissue-specific gene, uncoupling protein 1, is increased by the presence of TNF-alpha. The antiadipogenic effect of TNF-alpha was accompanied by a down-regulation of CCAAT/enhancer-binding protein-alpha and beta mRNAs and up-regulation of CCAAT/enhancer-binding protein-delta, with the expression of peroxisome proliferator-activated receptor-gamma remaining essentially unmodified. Moreover, TNF-alpha caused an insulin resistance on the insulin-induced glucose uptake in brown adipocytes. Pretreatment with TNF-alpha resulted in hypophosphorylation of the insulin receptor in response to insulin, without affecting the number of insulin receptors per cell or its molecular mass. However, insulin receptor substrate (IRS)-1 and IRS-2 signaling in response to insulin showed functional differences. Thus, TNF-alpha pretreatment induced a hypophosphorylation of IRS-2 but not of IRS-1. This effect leads to an impairment in the IRS-2-associated phosphatidylinositol (PI) 3-kinase activation due to a decreased association of alpha-p85 regulatory subunit of PI 3-kinase with IRS-2 but not in the IRS-1-associated PI 3-kinase activation in response to insulin. Our results indicate that TNF-alpha induced an IRS-2- but not IRS-1-mediated insulin resistance on glucose transport and lipid synthesis in fetal brown adipocytes. | lld:pubmed |
| pubmed-article:9492058 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9492058 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9492058 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:9492058 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9492058 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9492058 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:9492058 | pubmed:issn | 0013-7227 | lld:pubmed |
| pubmed-article:9492058 | pubmed:author | pubmed-author:BenitoMM | lld:pubmed |
| pubmed-article:9492058 | pubmed:author | pubmed-author:LorenziGG | lld:pubmed |
| pubmed-article:9492058 | pubmed:author | pubmed-author:ValverdeA MAM | lld:pubmed |
| pubmed-article:9492058 | pubmed:author | pubmed-author:NavarroPP | lld:pubmed |
| pubmed-article:9492058 | pubmed:author | pubmed-author:TeruelTT | lld:pubmed |
| pubmed-article:9492058 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9492058 | pubmed:volume | 139 | lld:pubmed |
| pubmed-article:9492058 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9492058 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9492058 | pubmed:pagination | 1229-38 | lld:pubmed |
| pubmed-article:9492058 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:9492058 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9492058 | pubmed:articleTitle | Tumor necrosis factor-alpha causes insulin receptor substrate-2-mediated insulin resistance and inhibits insulin-induced adipogenesis in fetal brown adipocytes. | lld:pubmed |
| pubmed-article:9492058 | pubmed:affiliation | Departamento de Bioquimica y Biologia Molecular II, Facultad de Farmacia, Universidad Complutense, Madrid, Spain. | lld:pubmed |
| pubmed-article:9492058 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9492058 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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