Hyperlipoproteinemia: Metabolic basis and rationale for therapy

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Most forms of hyperlipoproteinemia are the result of at least 1 of 4 basic defects of lipoprotein metabolism. Hypercholesterolemia is most commonly due to decreased activity of receptors for low-density lipoproteins (LDL). A deficiency of LDL receptors can be caused by either a genetic defect in the structure of the receptor or metabolic suppression of receptor synthesis by genetic factors or dietary saturated fatty acids and cholesterol. An elevation of triglycerides in chylomicrons or very low density lipoproteins (VLDL) can be secondary to a reduced activity of lipoprotein lipase, and an increase in the catabolic remnants of these lipoproteins can be due to an abnormal isoform of apolipoprotein E, the apolipoprotein that mediates hepatic uptake of lipoprotein remnants. Finally, hepatic overproduction of VLDL can produce hypertriglyceridemia, or if there is a concomitant defect in clearance of lipoproteins, an accentuated increase of VLDL, remnants or LDL will occur. Thus, lipoprotein overproduction can give rise to multiple lipoprotein phenotypes in a single family. Specific therapy of hyperlipoproteinemia should be directed toward correcting these metabolic defects.

Original languageEnglish (US)
Pages (from-to)20-26
Number of pages7
JournalThe American Journal of Cardiology
Volume54
Issue number5
DOIs
StatePublished - Aug 27 1984

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Hyperlipoproteinemias
Lipoproteins
VLDL Lipoproteins
LDL Receptors
Therapeutics
Chylomicrons
Lipoprotein Lipase
Apolipoproteins
Hypertriglyceridemia
Liver
Apolipoproteins E
Hypercholesterolemia
LDL Lipoproteins
Protein Isoforms
Triglycerides
Fatty Acids
Cholesterol
Phenotype

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Hyperlipoproteinemia : Metabolic basis and rationale for therapy. / Grundy, Scott M.

In: The American Journal of Cardiology, Vol. 54, No. 5, 27.08.1984, p. 20-26.

Research output: Contribution to journalArticle

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