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Article

Increased production of VLDL apoB-100 in subjects with familial hypercholesterolemia carrying the same null LDL receptor gene mutation.

Journal of lipid research - 1 May 2004

Tremblay André J, Lamarche Benoît, Ruel Isabelle L, Hogue Jean-Charles, Bergeron Jean, Gagné Claude, Couture Patrick

Abstract excerpt

Early radiokinetic studies revealed that the classical metabolic defect in patients with familial hypercholesterolemia (FH) is hypocatabolism of LDL due to decreased LDL receptor activity. However, recent studies have suggested that hepatic oversecretion of apolipoprotein B-100 (apoB-100)-containing lipoproteins could also contribute to the markedly elevated plasma concentrations of LDL-cholesterol found in FH....

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Identifiers

PMID: 14967814
DOI: 10.1194/jlr.M300448-JLR200

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Increased production of VLDL apoB-100 in subjects with familial hypercholesterolemia carrying the same null LDL receptor gene mutation.PMID 14967814Read ↗

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