Source:http://linkedlifedata.com/resource/pubmed/id/12454276
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2002-11-27
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pubmed:abstractText |
Apolipoprotein C-I (apoC-I) has been proposed to act primarily via interference with apoE-mediated lipoprotein uptake. To define actions of apoC-I that are independent of apoE, we crossed a moderately overexpressing human apoC-I transgenic, which possesses a minimal phenotype in the WT background, with the apoE-null mouse. Surprisingly, apoE-null/C-I mice showed much more severe hyperlipidemia than apoE-null littermates in both the fasting and non-fasting states, with an almost doubling of cholesterol, primarily in IDL+LDL, and a marked increase in triglycerides; 3-fold in females to 260 +/- 80 mg/dl and 14-fold in males to 1409 +/- 594 mg/dl. HDL lipids were not significantly altered but HDL were apoC-I-enriched and apoA-II-depleted. Production rates of VLDL triglyceride were unchanged as was the clearance of post-lipolysis remnant particles. Plasma post-heparin hepatic lipase and lipoprotein lipase levels were undiminished as was the in vitro hydrolysis of apoC-I transgenic VLDL. However, HDL from apoC-I transgenic mice had a marked inhibitory effect on hepatic lipase activity, as did purified apoC-I. LPL activity was minimally affected. Atherosclerosis assay revealed significantly increased atherosclerosis in apoE-null/C-I mice assessed via the en face assay. Inhibition of hepatic lipase may be an important mechanism of the decrease in lipoprotein clearance mediated by apoC-I.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoprotein C-I,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins C,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins E,
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol, VLDL,
http://linkedlifedata.com/resource/pubmed/chemical/Lipase,
http://linkedlifedata.com/resource/pubmed/chemical/Lipids
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pubmed:status |
MEDLINE
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pubmed:author | |
pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2136-45
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pubmed:dateRevised |
2007-11-14
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pubmed:articleTitle |
Overexpression of apoC-I in apoE-null mice: severe hypertriglyceridemia due to inhibition of hepatic lipase.
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pubmed:affiliation |
Department of Medicine, Columbia University, 630 W. 168th Street, New York, NY, USA.
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