Linked Life Data

6930928

Source:http://linkedlifedata.com/resource/pubmed/id/6930928

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1980-9-26
pubmed:abstractText
Action of LCAT on the plasma of patients afflicted with familial LCAT deficiency shifts the distribution of C apolipoproteins from lipoproteins of d less than 1.019 g/ml to lipoproteins of d greater than 1.109 g/ml, and causes an opposite shift in the distribution of apolipoprotein E. The altered distribution of apolipoprotein E appears to depend primarily on enzyme-related effects on HDL. Loss of apolipoprotein E from HDL occurs as cholesteryl esters are formed and transfer to other lipoproteins; disc-shaped HDL, rich in apolipoprotein E, are converted into spherical particles; and the population of HDL as a whole is converted first into particles the size of HDL2 and HDL3 and then into intermediate-sized particles. Transfer of apolipoprotein E to artificially prepared triglyceride-rich particles occurs at a nearly linear rate that is slow than the rates of formation and transfer of cholesteryl esters or the rate of formation of "HDL2" and "HDL3." Transfer of apolipoprotein E is faster, however, when the patients' disc-shaped HDL are incubated with triglyceride-rich particles in the presence of normal plasma lipoproteins of d greater than 1.063 g/ml. Since the disc-shaped HDL, rich in apolipoprotein E, resemble particles reported to be released from perfused rat livers, they may be nascent lipoproteins of hepatic origin. If so, it appears that action of LCAT on these lipoproteins may be one of the factors that regulates the content of apolipoprotein E in VLDL.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
348
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
224-43
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
In vitro effects of lecithin:cholesterol acyltransferase on apolipoprotein distribution in familial lecithin:cholesterol acyltransferase deficiency.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.