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Cited by 405

The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.

Polymorphism of apolipoprotein E: Genetics of hyperlipoproteinemia type III

Utermann, G., Vogelberg, K. H., Steinmetz, A., Schoenborn, W., Pruin, N., Jaeschke, M., Hees, M., Canzler, H.·1979·Clinical Genetics
DOI 10.1111/j.1399-0004.1979.tb02027.x
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Abstract

Apolipoprotein E from human serum shows a genetic polymorphism determined by two autosomal codominant alleles, Apo En and Apo E d. Homozygosity for the gene Apo E d (phenotype Apo E‐D) results in primary dysbetalipoproteinemia, but only some individuals with this phenotype develop gross hyperlipidemia (hyperlipoproteinemia type III). Vertical transmission of dysbetalipoproteinemia represents pseudodominance due to the high frequency of the gene Apo Ed. Dysbetalipoproteinemia is already expressed in childhood. To assess the influence of other genes on the expression of hyperlipidemia in phenotype Apo E‐D, comparative studies were carried out in kindreds of hypercholesterolemic (group A) and normo‐ or hypocholesterolemic probands with dysbetalipoproteinemia (group B). This demonstrated the occurrence of familial (non‐type III) forms of hyperlipidemia in group A but not in group B kindreds. Distribution of lipoprotein pheno‐types in five of the group A kindreds was consistent with the occurrence of familial combined hyperlipidemia. Apo E phenotypes and hyperlipidemia segregated independently. It is concluded that primary dysbetalipoproteinemia is a frequent monogenic variant of lipoprotein metabolism, but not a disease. Coincidence in one individual of genes for this specific dyslipoproteinemia with any of the genes for monogenic or polygenic forms of familial hyperlipidemia results in hyperlipoproteinemia type III. Hence hyperlipoproteinemia type III is caused by at least two non‐allelic genes and is a polygenic disorder.

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Citations

Cites

Research works printed but not linked: 11

  1. Bilheimer D. W., 1971, Abnormal metabolism of very low density lipoproteins in type 111, Circulation, 44, 11
  2. Gofman J. W., 1956, The serum lipoprotein transport system in health, metabolic disorder, atherosclerosis and coronary artery disease, Plasma, 2, 413
  3. Hall M. H., 1974, A mathematical model for apoprotein kinetics in normal and hyperlipidemic patients, Circulation, 114
  4. Havel R. J., 1969, Advances in Internal Medicine, 117
  5. Hazzard W. R., 1971, Impaired removal of very low density lipoprotein (VLDL) “remnants” in the pathogenesis of broad‐beta disease (type III hyperlipoproteinemia), Clin. Res., 19, 476
  6. 10.1111/j.1399-0004.1976.tb01554.x · doi:10.1111/j.1399-0004.1976.tb01554.x
  7. Lasser N. L., 1972, The occurrence of type III and type II hyperlipoproteinemia in a single kindred, Clin. Res., 20
  8. Mishkel M. A., 1971, Protides of the Biological Fluids, 283
  9. Moser H., 1974, Atherosclerosis, 854
  10. Namboodiri K. K., 1975, Bivariate analyses of cholesterol and triglyceride levels in families in which probands have type lib lipoprotein phenotype, Amer. J. hum. Genet., 27, 454
  11. Utermann G., 1977, Protides of the Biological Fluids, 285

Cited by

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Metadata

Authors
Utermann, G., Vogelberg, K. H., Steinmetz, A., Schoenborn, W., Pruin, N., Jaeschke, M., Hees, M., & Canzler, H.
Venue
Clinical Genetics
Publisher
Wiley
Published
1979-01
Volume
15
Issue
1
Pages
37-62
ISSN
  • 0009-9163 (ISSN-L)
  • 1399-0004
DOI
10.1111/j.1399-0004.1979.tb02027.x
OpenAlex
W1991306495
Cited by
405
References
36
FWCI
16.29
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 10705 d)

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