| pubmed-article:11027633 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11027633 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:11027633 | lifeskim:mentions | umls-concept:C0028754 | lld:lifeskim |
| pubmed-article:11027633 | lifeskim:mentions | umls-concept:C0299250 | lld:lifeskim |
| pubmed-article:11027633 | lifeskim:mentions | umls-concept:C0206131 | lld:lifeskim |
| pubmed-article:11027633 | lifeskim:mentions | umls-concept:C0299583 | lld:lifeskim |
| pubmed-article:11027633 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:11027633 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:11027633 | pubmed:dateCreated | 2000-12-7 | lld:pubmed |
| pubmed-article:11027633 | pubmed:abstractText | Liver-derived hyperleptinemia induced in normal rats by adenovirus-induced gene transfer causes rapid disappearance of body fat, whereas the endogenous adipocyte-derived hyperleptinemia of obesity does not. Here we induce liver-derived hyperleptinemia in rats with adipocyte-derived hyperleptinemia of acquired obesity caused by ventromedial hypothalamus lesioning (VMH rats) or by feeding 60% fat (DIO rats). Liver-derived hyperleptinemia in obese rats caused only a 5-7% loss of body weight, compared to a 13% loss in normoleptinemic lean animals; but in actual grams of weight lost there was no significant difference between obese and lean groups, suggesting that a subset of cells remain leptin-sensitive in obesity. mRNA and protein of a putative leptin-resistance factor, suppressor of cytokine signaling (SOCS)-1 or -3, were both increased in white adipose tissues (WAT) of VMH and DIO rats. Since transgenic overexpression of SOCS-3 in islets reduced the lipopenic effect of leptin by 75%, we conclude that the increased expression of SOCS-1 and -3 in WAT of rats with acquired obesity could have blocked leptin's lipopenic action in the leptin-resistant WAT population. | lld:pubmed |
| pubmed-article:11027633 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11027633 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11027633 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11027633 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11027633 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11027633 | pubmed:issn | 0006-291X | lld:pubmed |
| pubmed-article:11027633 | pubmed:author | pubmed-author:LeoCC | lld:pubmed |
| pubmed-article:11027633 | pubmed:author | pubmed-author:KalraS PSP | lld:pubmed |
| pubmed-article:11027633 | pubmed:author | pubmed-author:KalraP SPS | lld:pubmed |
| pubmed-article:11027633 | pubmed:author | pubmed-author:UngerR HRH | lld:pubmed |
| pubmed-article:11027633 | pubmed:author | pubmed-author:WangZZ | lld:pubmed |
| pubmed-article:11027633 | pubmed:author | pubmed-author:PaiRR | lld:pubmed |
| pubmed-article:11027633 | pubmed:author | pubmed-author:KakumaTT | lld:pubmed |
| pubmed-article:11027633 | pubmed:author | pubmed-author:ZhouY TYT | lld:pubmed |
| pubmed-article:11027633 | pubmed:copyrightInfo | Copyright 2000 Academic Press. | lld:pubmed |
| pubmed-article:11027633 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11027633 | pubmed:day | 14 | lld:pubmed |
| pubmed-article:11027633 | pubmed:volume | 277 | lld:pubmed |
| pubmed-article:11027633 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11027633 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11027633 | pubmed:pagination | 20-6 | lld:pubmed |
| pubmed-article:11027633 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:11027633 | pubmed:meshHeading | pubmed-meshheading:11027633... | lld:pubmed |
| pubmed-article:11027633 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11027633 | pubmed:articleTitle | Leptin resistance of adipocytes in obesity: role of suppressors of cytokine signaling. | lld:pubmed |
| pubmed-article:11027633 | pubmed:affiliation | Gifford Laboratories, Touchstone Center for Diabetes Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA. | lld:pubmed |
| pubmed-article:11027633 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11027633 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11027633 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:11027633 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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