Source:http://linkedlifedata.com/resource/pubmed/id/17183024
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2007-2-22
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pubmed:abstractText |
To better understand the role of LCAT in HDL metabolism, we compared HDL subpopulations in subjects with homozygous (n = 11) and heterozygous (n = 11) LCAT deficiency with controls (n = 22). Distribution and concentrations of apolipoprotein A-I (apoA-I)-, apoA-II-, apoA-IV-, apoC-I-, apoC-III-, and apoE-containing HDL subpopulations were assessed. Compared with controls, homozygotes and heterozygotes had lower LCAT masses (-77% and -13%), and LCAT activities (-99% and -39%), respectively. In homozygotes, the majority of apoA-I was found in small, disc-shaped, poorly lipidated prebeta-1 and alpha-4 HDL particles, and some apoA-I was found in larger, lipid-poor, discoidal HDL particles with alpha-mobility. No apoC-I-containing HDL was noted, and all apoA-II and apoC-III was detected in lipid-poor, prebeta-mobility particles. ApoE-containing particles were more disperse than normal. ApoA-IV-containing particles were normal. Heterozygotes had profiles similar to controls, except that apoC-III was found only in small HDL with prebeta-mobility. Our data are consistent with the concepts that LCAT activity: 1) is essential for developing large, spherical, apoA-I-containing HDL and for the formation of normal-sized apoC-I and apoC-III HDL; and 2) has little affect on the conversion of prebeta-1 into alpha-4 HDL, only slight effects on apoE HDL, and no effect on apoA-IV HDL particles.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoprotein A-I,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoprotein A-II,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoprotein C-I,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoprotein C-III,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins A,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins E,
http://linkedlifedata.com/resource/pubmed/chemical/Lipoproteins, HDL,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylcholine-Sterol...
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-2275
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
48
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
592-9
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pubmed:dateRevised |
2007-12-3
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pubmed:meshHeading |
pubmed-meshheading:17183024-Analysis of Variance,
pubmed-meshheading:17183024-Apolipoprotein A-I,
pubmed-meshheading:17183024-Apolipoprotein A-II,
pubmed-meshheading:17183024-Apolipoprotein C-I,
pubmed-meshheading:17183024-Apolipoprotein C-III,
pubmed-meshheading:17183024-Apolipoproteins A,
pubmed-meshheading:17183024-Apolipoproteins E,
pubmed-meshheading:17183024-Female,
pubmed-meshheading:17183024-Heterozygote,
pubmed-meshheading:17183024-Homozygote,
pubmed-meshheading:17183024-Humans,
pubmed-meshheading:17183024-Lecithin Acyltransferase Deficiency,
pubmed-meshheading:17183024-Lipoproteins, HDL,
pubmed-meshheading:17183024-Male,
pubmed-meshheading:17183024-Models, Biological,
pubmed-meshheading:17183024-Phosphatidylcholine-Sterol O-Acyltransferase
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pubmed:year |
2007
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pubmed:articleTitle |
Role of LCAT in HDL remodeling: investigation of LCAT deficiency states.
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pubmed:affiliation |
Lipid Metabolism Laboratory, Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA. bela.asztalos@tufts.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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