pubmed-article:19151202 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19151202 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:19151202 | lifeskim:mentions | umls-concept:C0299583 | lld:lifeskim |
pubmed-article:19151202 | lifeskim:mentions | umls-concept:C0017725 | lld:lifeskim |
pubmed-article:19151202 | lifeskim:mentions | umls-concept:C0312418 | lld:lifeskim |
pubmed-article:19151202 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
pubmed-article:19151202 | lifeskim:mentions | umls-concept:C0036667 | lld:lifeskim |
pubmed-article:19151202 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:19151202 | pubmed:dateCreated | 2009-4-1 | lld:pubmed |
pubmed-article:19151202 | pubmed:abstractText | Ghrelin is the only known peripheral hormone to increase ingestive behavior. However, its role in the physiological regulation of energy homeostasis is unclear because deletion of ghrelin or its receptor does not alter food intake or body weight in mice fed a normal chow diet. We hypothesized that overexpression of ghrelin in its physiological tissues would increase food intake and body weight. | lld:pubmed |
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pubmed-article:19151202 | pubmed:language | eng | lld:pubmed |
pubmed-article:19151202 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19151202 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:19151202 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19151202 | pubmed:month | Apr | lld:pubmed |
pubmed-article:19151202 | pubmed:issn | 1939-327X | lld:pubmed |
pubmed-article:19151202 | pubmed:author | pubmed-author:GhateiMohamme... | lld:pubmed |
pubmed-article:19151202 | pubmed:author | pubmed-author:BloomStephen... | lld:pubmed |
pubmed-article:19151202 | pubmed:author | pubmed-author:PattersonMich... | lld:pubmed |
pubmed-article:19151202 | pubmed:author | pubmed-author:GardinerJames... | lld:pubmed |
pubmed-article:19151202 | pubmed:author | pubmed-author:BewickGavin... | lld:pubmed |
pubmed-article:19151202 | pubmed:author | pubmed-author:CampbellDanie... | lld:pubmed |
pubmed-article:19151202 | pubmed:author | pubmed-author:KentAyshaA | lld:pubmed |
pubmed-article:19151202 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19151202 | pubmed:volume | 58 | lld:pubmed |
pubmed-article:19151202 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19151202 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19151202 | pubmed:pagination | 840-6 | lld:pubmed |
pubmed-article:19151202 | pubmed:dateRevised | 2010-9-23 | lld:pubmed |
pubmed-article:19151202 | pubmed:meshHeading | pubmed-meshheading:19151202... | lld:pubmed |
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pubmed-article:19151202 | pubmed:meshHeading | pubmed-meshheading:19151202... | lld:pubmed |
pubmed-article:19151202 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19151202 | pubmed:articleTitle | Mice with hyperghrelinemia are hyperphagic and glucose intolerant and have reduced leptin sensitivity. | lld:pubmed |
pubmed-article:19151202 | pubmed:affiliation | Department of Investigative Medicine, Hammersmith Campus, Imperial College London, London, UK. | lld:pubmed |
pubmed-article:19151202 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19151202 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:58991 | entrezgene:pubmed | pubmed-article:19151202 | lld:entrezgene |
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