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Article

Lack of evidence for reduced plasma apo B48 catabolism in patients with heterozygous familial hypercholesterolemia carrying the same null LDL receptor gene mutation.

Atherosclerosis - 1 Feb 2004

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

Abstract excerpt

Increasing evidence suggests that remnants of chylomicrons and very low density lipoprotein (VLDL) also known as triglyceride-rich lipoproteins (TRL) are directly related to the pathogenesis of atherosclerosis. While studies in animals suggest that low density lipoprotein (LDL) receptor deficiency delays clearance of chylomicron remnants, human data supporting this hypothesis are conflicting. The objective of...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 15019548
DOI: 10.1016/j.atherosclerosis.2003.11.011

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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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Lack of evidence for reduced plasma apo B48 catabolism in patients with heterozygous familial hypercholesterolemia carrying the same null LDL receptor gene mutation.PMID 15019548Read ↗

The removal from plasma of chylomicrons and remnants is reduced in heterozygous familial hypercholesterolemia subjects with identified LDL receptor mutations: study with artificial emulsions.Semantic proximity Read ↗

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

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Low rate of production of apolipoproteins B100 and AI in 2 patients with Anderson disease (chylomicron retention disease).Semantic proximity Read ↗

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