| pubmed-article:8876155 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8876155 | lifeskim:mentions | umls-concept:C0034493 | lld:lifeskim |
| pubmed-article:8876155 | lifeskim:mentions | umls-concept:C0003069 | lld:lifeskim |
| pubmed-article:8876155 | lifeskim:mentions | umls-concept:C0004153 | lld:lifeskim |
| pubmed-article:8876155 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:8876155 | lifeskim:mentions | umls-concept:C1416804 | lld:lifeskim |
| pubmed-article:8876155 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
| pubmed-article:8876155 | pubmed:issue | 21 | lld:pubmed |
| pubmed-article:8876155 | pubmed:dateCreated | 1996-12-4 | lld:pubmed |
| pubmed-article:8876155 | pubmed:abstractText | Lecithin:cholesterol acyltransferase (LCAT) is a key plasma enzyme in cholesterol and high density lipoprotein (HDL) metabolism. Transgenic rabbits overexpressing human LCAT had 15-fold greater plasma LCAT activity that nontransgenic control rabbits. This degree of overexpression was associated with a 6.7-fold increase in the plasma HDL cholesterol concentration in LCAT transgenic rabbits. On a 0.3% cholesterol diet, the HDL cholesterol concentrations increased from 24 +/- 1 to 39 +/- 3 mg/dl in nontransgenic control rabbits (n = 10; P < 0.05) and increased from 161 +/- 5 to 200 +/- 21 mg/dl (P < 0.001) in the LCAT transgenic rabbits (n = 9). Although the baseline non-HDL concentrations of control (4 +/- 3 mg/dl) and transgenic rabbits (18 +/- 4 mg/dl) were similar, the cholesterol-rich diet raised the non-HDL cholesterol concentrations, reflecting the atherogenic very low density, intermediate density, and low density lipoprotein particles observed by gel filtration chromatography. The non-HDL cholesterol rose to 509 +/- 57 mg/dl in controls compared with only 196 +/- 14 mg/dl in the LCAT transgenic rabbits (P < 0.005). The differences in the plasma lipoprotein response to a cholesterol-rich diet observed in the transgenic rabbits paralleled the susceptibility to developing aortic atherosclerosis. Compared with nontransgenic controls, LCAT transgenic rabbits were protected from diet-induced atherosclerosis with significant reductions determined by both quantitative planimetry (-86%; P < 0.003) and quantitative immunohistochemistry (-93%; P < 0.009). Our results establish the importance of LCAT in the metabolism of both HDL and apolipoprotein B-containing lipoprotein particles with cholesterol feeding and the response to diet-induced atherosclerosis. In addition, these findings identify LCAT as a new target for therapy to prevent atherosclerosis. | lld:pubmed |
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| pubmed-article:8876155 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8876155 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8876155 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8876155 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:8876155 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:BrewerH BHBJr | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:CornhillJ FJF | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:HoytR FRFJr | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:HaudenschildC... | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:HoegJ MJM | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:VaismanB LBL | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:HerderickE... | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:FeldmanS HSH | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:Santamarina-F... | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:MarcovinaS... | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:DemoskyS... | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:HazelC MCM | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:BérardA MAM | lld:pubmed |
| pubmed-article:8876155 | pubmed:author | pubmed-author:KauffmanR DRD | lld:pubmed |
| pubmed-article:8876155 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8876155 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:8876155 | pubmed:volume | 93 | lld:pubmed |
| pubmed-article:8876155 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8876155 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8876155 | pubmed:pagination | 11448-53 | lld:pubmed |
| pubmed-article:8876155 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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