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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1990-8-13
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pubmed:abstractText |
The inheritance of low density lipoprotein (LDL) subclass patterns was investigated in 234 members of seven large kindreds with familial combined hyperlipidemia (FCHL), a disorder characterized by elevated LDL cholesterol and/or triglyceride and increased coronary disease risk in families. Analysis of LDL subclasses by nondenaturing gradient gel electrophoresis showed a predominance of large, buoyant LDL particles (pattern A) in 71% of the family members and a predominance of small, dense LDL particles (pattern B) in 29% of family members. Based on complex segregation analysis, pattern B appeared to be inherited as an autosomal trait with either a dominant or an additive mode of inheritance and a small, but significant, multifactorial inheritance component. The proposed allele for pattern B was common (frequency = 0.3), and reduced penetrance was observed among men under age 20 and among women under age 50. These results in these FCHL families are consistent with those from a previously reported population-based sample of families, in which pattern B showed an apparent dominant mode of inheritance. In that study, reduced penetrance was observed for men under age 20 and for premenopausal women, but a somewhat lower allele frequency was found for pattern B (0.25). In the FCHL family members, LDL subclass pattern B was associated with significantly increased plasma levels of apolipoprotein B and triglyceride and decreased high density lipoprotein cholesterol. In comparison with a group of controls, the FCHL family members with pattern A had similar mean triglyceride levels, but higher mean apolipoprotein B. Thus, in families with FCHL, a predominance of small, dense LDL particles appears to be inherited as a common, single-gene trait, which is closely associated with the higher plasma triglyceride levels found in these families. The increased plasma apolipoprotein B levels found in FCHL cannot, however, be accounted for by this proposed locus.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0276-5047
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
520-30
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2369363-Adult,
pubmed-meshheading:2369363-Apolipoproteins B,
pubmed-meshheading:2369363-Female,
pubmed-meshheading:2369363-Genotype,
pubmed-meshheading:2369363-Humans,
pubmed-meshheading:2369363-Hyperlipidemia, Familial Combined,
pubmed-meshheading:2369363-Lipoproteins, LDL,
pubmed-meshheading:2369363-Male,
pubmed-meshheading:2369363-Middle Aged,
pubmed-meshheading:2369363-Models, Statistical,
pubmed-meshheading:2369363-Pedigree
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pubmed:articleTitle |
Inheritance of low density lipoprotein subclass patterns in familial combined hyperlipidemia.
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pubmed:affiliation |
Department of Epidemiology, University of Washington, Seattle 98195.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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