| pubmed-article:12730242 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12730242 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
| pubmed-article:12730242 | lifeskim:mentions | umls-concept:C0206131 | lld:lifeskim |
| pubmed-article:12730242 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:12730242 | lifeskim:mentions | umls-concept:C0123658 | lld:lifeskim |
| pubmed-article:12730242 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:12730242 | pubmed:issue | 29 | lld:pubmed |
| pubmed-article:12730242 | pubmed:dateCreated | 2003-7-14 | lld:pubmed |
| pubmed-article:12730242 | pubmed:abstractText | In 3T3-L1 adipocytes, hyperosmotic stress was found to inhibit insulin signaling, leading to an insulin-resistant state. We show here that, despite normal activation of insulin receptor, hyperosmotic stress inhibits both tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1-associated phosphoinositide 3 (PI 3)-kinase activity in response to physiological insulin concentrations. Insulin-induced membrane ruffling, which is dependent on PI 3-kinase activation, was also markedly reduced. These inhibitory effects were associated with an increase in IRS-1 Ser307 phosphorylation. Furthermore, the mammalian target of rapamycin (mTOR) inhibitor rapamycin prevented the osmotic shock-induced phosphorylation of IRS-1 on Ser307. The inhibition of mTOR completely reversed the inhibitory effect of hyperosmotic stress on insulin-induced IRS-1 tyrosine phosphorylation and PI 3-kinase activation. In addition, prolonged osmotic stress enhanced the degradation of IRS proteins through a rapamycin-insensitive pathway and a proteasome-independent process. These data support evidence of new mechanisms involved in osmotic stress-induced cellular insulin resistance. Short-term osmotic stress induces the phosphorylation of IRS-1 on Ser307 by an mTOR-dependent pathway. This, in turn, leads to a decrease in early proximal signaling events induced by physiological insulin concentrations. On the other hand, prolonged osmotic stress alters IRS-1 function by inducing its degradation, which could contribute to the down-regulation of insulin action. | lld:pubmed |
| pubmed-article:12730242 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12730242 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12730242 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12730242 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12730242 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:12730242 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:12730242 | pubmed:author | pubmed-author:Le... | lld:pubmed |
| pubmed-article:12730242 | pubmed:author | pubmed-author:GonzalezTeres... | lld:pubmed |
| pubmed-article:12730242 | pubmed:author | pubmed-author:GualPhilippeP | lld:pubmed |
| pubmed-article:12730242 | pubmed:author | pubmed-author:GrémeauxThier... | lld:pubmed |
| pubmed-article:12730242 | pubmed:author | pubmed-author:TantiJean-Fra... | lld:pubmed |
| pubmed-article:12730242 | pubmed:author | pubmed-author:BarresRomainR | lld:pubmed |
| pubmed-article:12730242 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12730242 | pubmed:day | 18 | lld:pubmed |
| pubmed-article:12730242 | pubmed:volume | 278 | lld:pubmed |
| pubmed-article:12730242 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12730242 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12730242 | pubmed:pagination | 26550-7 | lld:pubmed |
| pubmed-article:12730242 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:12730242 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12730242 | pubmed:articleTitle | Hyperosmotic stress inhibits insulin receptor substrate-1 function by distinct mechanisms in 3T3-L1 adipocytes. | lld:pubmed |
| pubmed-article:12730242 | pubmed:affiliation | INSERM U 568 and l'Institut Fédératif de Recherches 50, Faculté de Médecine, Avenue de Valombrose, 06107 Nice Cedex 02, France. | lld:pubmed |
| pubmed-article:12730242 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12730242 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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