| pubmed-article:10899071 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10899071 | lifeskim:mentions | umls-concept:C0033085 | lld:lifeskim |
| pubmed-article:10899071 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:10899071 | lifeskim:mentions | umls-concept:C0333959 | lld:lifeskim |
| pubmed-article:10899071 | lifeskim:mentions | umls-concept:C0596620 | lld:lifeskim |
| pubmed-article:10899071 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:10899071 | pubmed:dateCreated | 2000-8-16 | lld:pubmed |
| pubmed-article:10899071 | pubmed:abstractText | GLUT4-null mice lacking the insulin-sensitive glucose transporter are not diabetic but do exhibit abnormalities in glucose and lipid metabolism. The most striking morphological consequence of ablating GLUT4 is cardiac hypertrophy. GLUT4-null hearts display characteristics of hypertrophy caused by hypertension. However, GLUT4-null mice have normal blood pressure and maintain a normal cardiac contractile protein profile. Unexpectedly, although they lack the predominant glucose transporter in the heart, GLUT4-null hearts transport glucose and synthesize glycogen at normal levels, but gene expression of rate-limiting enzymes involved in fatty acid oxidation is decreased. The GLUT4-null heart represents a unique model of hypertrophy that may be used to study the consequences of altered substrate utilization in normal and pathophysiological conditions. | lld:pubmed |
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| pubmed-article:10899071 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10899071 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10899071 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10899071 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10899071 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:10899071 | pubmed:issn | 0363-6135 | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:KatsE IEI | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:MalhotraAA | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:FactorS MSM | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:PECORALL | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:ChathamJ CJC | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:ChackoV PVP | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:JelicksL ALA | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:CharronM JMJ | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:GeenenD LDL | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:WeissR GRG | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:TsaiT YTY | lld:pubmed |
| pubmed-article:10899071 | pubmed:author | pubmed-author:StenbitA EAE | lld:pubmed |
| pubmed-article:10899071 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10899071 | pubmed:volume | 279 | lld:pubmed |
| pubmed-article:10899071 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10899071 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10899071 | pubmed:pagination | H313-8 | lld:pubmed |
| pubmed-article:10899071 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:10899071 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10899071 | pubmed:articleTitle | Preservation of glucose metabolism in hypertrophic GLUT4-null hearts. | lld:pubmed |
| pubmed-article:10899071 | pubmed:affiliation | Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York 10461-1602, USA. | lld:pubmed |
| pubmed-article:10899071 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10899071 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10899071 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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