| pubmed-article:20852327 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20852327 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:20852327 | lifeskim:mentions | umls-concept:C0015684 | lld:lifeskim |
| pubmed-article:20852327 | lifeskim:mentions | umls-concept:C0023779 | lld:lifeskim |
| pubmed-article:20852327 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:20852327 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:20852327 | lifeskim:mentions | umls-concept:C0243144 | lld:lifeskim |
| pubmed-article:20852327 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:20852327 | lifeskim:mentions | umls-concept:C1521975 | lld:lifeskim |
| pubmed-article:20852327 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:20852327 | pubmed:issue | 49 | lld:pubmed |
| pubmed-article:20852327 | pubmed:dateCreated | 2010-11-29 | lld:pubmed |
| pubmed-article:20852327 | pubmed:abstractText | Lipids circulate in the blood in association with plasma lipoproteins and enter the tissues either after hydrolysis or as non-hydrolyzable lipid esters. We studied cardiac lipids, lipoprotein lipid uptake, and gene expression in heart-specific lipoprotein lipase (LpL) knock-out (hLpL0), CD36 knock-out (Cd36(-/-)), and double knock-out (hLpL0/Cd36(-/-)-DKO) mice. Loss of either LpL or CD36 led to a significant reduction in heart total fatty acyl-CoA (control, 99.5 ± 3.8; hLpL0, 36.2 ± 3.5; Cd36(-/-), 57.7 ± 5.5 nmol/g, p < 0.05) and an additive effect was observed in the DKO (20.2 ± 1.4 nmol/g, p < 0.05). Myocardial VLDL-triglyceride (TG) uptake was reduced in the hLpL0 (31 ± 6%) and Cd36(-/-) (47 ± 4%) mice with an additive reduction in the DKO (64 ± 5%) compared with control. However, LpL but not CD36 deficiency decreased VLDL-cholesteryl ester uptake. Endogenously labeled mouse chylomicrons were produced by tamoxifen treatment of ?-actin-MerCreMer/LpL(flox/flox) mice. Induced loss of LpL increased TG levels >10-fold and reduced HDL by >50%. After injection of these labeled chylomicrons in the different mice, chylomicron TG uptake was reduced by ?70% and retinyl ester by ?50% in hLpL0 hearts. Loss of CD36 did not alter either chylomicron TG or retinyl ester uptake. LpL loss did not affect uptake of remnant lipoproteins from ApoE knock-out mice. Our data are consistent with two pathways for fatty acid uptake; a CD36 process for VLDL-derived fatty acid and a non-CD36 process for chylomicron-derived fatty acid uptake. In addition, our data show that lipolysis is involved in uptake of core lipids from TG-rich lipoproteins. | lld:pubmed |
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| pubmed-article:20852327 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20852327 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20852327 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20852327 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20852327 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20852327 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20852327 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20852327 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20852327 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:20852327 | pubmed:issn | 1083-351X | lld:pubmed |
| pubmed-article:20852327 | pubmed:author | pubmed-author:GoldbergIra... | lld:pubmed |
| pubmed-article:20852327 | pubmed:author | pubmed-author:ShulmanGerald... | lld:pubmed |
| pubmed-article:20852327 | pubmed:author | pubmed-author:HuYunyingY | lld:pubmed |
| pubmed-article:20852327 | pubmed:author | pubmed-author:AbumradNada... | lld:pubmed |
| pubmed-article:20852327 | pubmed:author | pubmed-author:RamakrishnanR... | lld:pubmed |
| pubmed-article:20852327 | pubmed:author | pubmed-author:BlanerWilliam... | lld:pubmed |
| pubmed-article:20852327 | pubmed:author | pubmed-author:HiyamaYaekoY | lld:pubmed |
| pubmed-article:20852327 | pubmed:author | pubmed-author:HugginsLesley... | lld:pubmed |
| pubmed-article:20852327 | pubmed:author | pubmed-author:BharadwajKaly... | lld:pubmed |
| pubmed-article:20852327 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20852327 | pubmed:day | 3 | lld:pubmed |
| pubmed-article:20852327 | pubmed:volume | 285 | lld:pubmed |
| pubmed-article:20852327 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20852327 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20852327 | pubmed:pagination | 37976-86 | lld:pubmed |
| pubmed-article:20852327 | pubmed:dateRevised | 2011-3-30 | lld:pubmed |
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| pubmed-article:20852327 | pubmed:meshHeading | pubmed-meshheading:20852327... | lld:pubmed |
| pubmed-article:20852327 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20852327 | pubmed:articleTitle | Chylomicron- and VLDL-derived lipids enter the heart through different pathways: in vivo evidence for receptor- and non-receptor-mediated fatty acid uptake. | lld:pubmed |
| pubmed-article:20852327 | pubmed:affiliation | Division of Preventive Medicine and Nutrition, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA. | lld:pubmed |
| pubmed-article:20852327 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20852327 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:20852327 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:20852327 | lld:pubmed |
