| pubmed-article:21592121 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21592121 | lifeskim:mentions | umls-concept:C0006104 | lld:lifeskim |
| pubmed-article:21592121 | lifeskim:mentions | umls-concept:C0025958 | lld:lifeskim |
| pubmed-article:21592121 | lifeskim:mentions | umls-concept:C0007258 | lld:lifeskim |
| pubmed-article:21592121 | lifeskim:mentions | umls-concept:C1274040 | lld:lifeskim |
| pubmed-article:21592121 | lifeskim:mentions | umls-concept:C0443281 | lld:lifeskim |
| pubmed-article:21592121 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:21592121 | pubmed:dateCreated | 2011-7-13 | lld:pubmed |
| pubmed-article:21592121 | pubmed:abstractText | Carnitine palmitoyltransferase-1c (CPT1c) is a newly identified and poorly understood brain-specific CPT1 homologue. Here, we have generated a new animal model that allows the conditional expression of CPT1c in a tissue specific and/or temporal manner via Cre-lox mediated recombination. Brain-specific, exogenous expression of CPT1c was achieved by crossing transgenic CPT1c mice to Nestin-Cre mice. The resulting double transgenic mice (CPT1c-TgN) displayed severe growth retardation in the postnatal period with a stunted development at 2 weeks of age. CPT1c-TgN mice had a greater than 2.3-fold reduction in brain weight. Even with this degree of microencephaly, CPT1c-TgN mice were viable and fertile and exhibited normal post-weaning growth. When fed a high fat diet CPT1c-TgN mice were protected from weight gain and the difference in body weight between CPT1c-TgN and control mice was further exaggerated. Conversely, low fat, high carbohydrate feeding partially reversed the body weight defects in CPT1c-TgN mice. Analysis of total brain lipids of low fat fed mice revealed a depletion of total very long chain fatty acids in adult CPT1c-TgN mice which was not evident in high fat fed CPT1c-TgN mice. These data show that CPT1c can elicit profound effects on brain physiology and total fatty acid profiles, which can be modulated by the nutritional composition of the diet. | lld:pubmed |
| pubmed-article:21592121 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21592121 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21592121 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:21592121 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21592121 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21592121 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21592121 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21592121 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21592121 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21592121 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:21592121 | pubmed:issn | 1471-4159 | lld:pubmed |
| pubmed-article:21592121 | pubmed:author | pubmed-author:WolfgangMicha... | lld:pubmed |
| pubmed-article:21592121 | pubmed:author | pubmed-author:ReamyAmanda... | lld:pubmed |
| pubmed-article:21592121 | pubmed:copyrightInfo | © 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry. | lld:pubmed |
| pubmed-article:21592121 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21592121 | pubmed:volume | 118 | lld:pubmed |
| pubmed-article:21592121 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21592121 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21592121 | pubmed:pagination | 388-98 | lld:pubmed |
| pubmed-article:21592121 | pubmed:meshHeading | pubmed-meshheading:21592121... | lld:pubmed |
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| pubmed-article:21592121 | pubmed:meshHeading | pubmed-meshheading:21592121... | lld:pubmed |
| pubmed-article:21592121 | pubmed:meshHeading | pubmed-meshheading:21592121... | lld:pubmed |
| pubmed-article:21592121 | pubmed:meshHeading | pubmed-meshheading:21592121... | lld:pubmed |
| pubmed-article:21592121 | pubmed:meshHeading | pubmed-meshheading:21592121... | lld:pubmed |
| pubmed-article:21592121 | pubmed:meshHeading | pubmed-meshheading:21592121... | lld:pubmed |
| pubmed-article:21592121 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21592121 | pubmed:articleTitle | Carnitine palmitoyltransferase-1c gain-of-function in the brain results in postnatal microencephaly. | lld:pubmed |
| pubmed-article:21592121 | pubmed:affiliation | Center for Metabolism and Obesity Research, Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. | lld:pubmed |
| pubmed-article:21592121 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21592121 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:78070 | entrezgene:pubmed | pubmed-article:21592121 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:21592121 | lld:entrezgene |
