| pubmed-article:12114623 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12114623 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:12114623 | lifeskim:mentions | umls-concept:C0043096 | lld:lifeskim |
| pubmed-article:12114623 | lifeskim:mentions | umls-concept:C0075202 | lld:lifeskim |
| pubmed-article:12114623 | pubmed:issue | 5579 | lld:pubmed |
| pubmed-article:12114623 | pubmed:dateCreated | 2002-7-12 | lld:pubmed |
| pubmed-article:12114623 | pubmed:abstractText | Leptin elicits a metabolic response that cannot be explained by its anorectic effects alone. To examine the mechanism underlying leptin's metabolic actions, we used transcription profiling to identify leptin-regulated genes in ob/ob liver. Leptin was found to specifically repress RNA levels and enzymatic activity of hepatic stearoyl-CoA desaturase-1 (SCD-1), which catalyzes the biosynthesis of monounsaturated fatty acids. Mice lacking SCD-1 were lean and hypermetabolic. ob/ob mice with mutations in SCD-1 were significantly less obese than ob/ob controls and had markedly increased energy expenditure. ob/ob mice with mutations in SCD-1 had histologically normal livers with significantly reduced triglyceride storage and VLDL (very low density lipoprotein) production. These findings suggest that down-regulation of SCD-1 is an important component of leptin's metabolic actions. | lld:pubmed |
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| pubmed-article:12114623 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12114623 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12114623 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12114623 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:12114623 | pubmed:issn | 1095-9203 | lld:pubmed |
| pubmed-article:12114623 | pubmed:author | pubmed-author:FriedmanJeffr... | lld:pubmed |
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| pubmed-article:12114623 | pubmed:author | pubmed-author:Hagge-Greenbe... | lld:pubmed |
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| pubmed-article:12114623 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12114623 | pubmed:day | 12 | lld:pubmed |
| pubmed-article:12114623 | pubmed:volume | 297 | lld:pubmed |
| pubmed-article:12114623 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12114623 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12114623 | pubmed:pagination | 240-3 | lld:pubmed |
| pubmed-article:12114623 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:12114623 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12114623 | pubmed:articleTitle | Role for stearoyl-CoA desaturase-1 in leptin-mediated weight loss. | lld:pubmed |
| pubmed-article:12114623 | pubmed:affiliation | Laboratory of Molecular Genetics, Center for Studies in Physics and Biology, Rogosin Institute, Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. | lld:pubmed |
| pubmed-article:12114623 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12114623 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12114623 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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