Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Severe hypertriglyceridemia in human APOC1 transgenic mice is caused by apoC-I-induced inhibition of LPL.

Journal of lipid research - 1 Feb 2005

Berbée Jimmy F P, van der Hoogt Caroline C, Sundararaman Deepa, Havekes Louis M, Rensen Patrick C N

Abstract excerpt

Studies in humans and mice have shown that increased expression of apolipoprotein C-I (apoC-I) results in combined hyperlipidemia with a more pronounced effect on triglycerides (TGs) compared with total cholesterol (TC). The aim of this study was to elucidate the main reason for this effect using human apoC-I-expressing (APOC1) mice. Moderate plasma human apoC-I levels (i.e., 4-fold higher than human levels)...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Apolipoproteins
Share to Apolipoproteins C

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hypertriglyceridemia

Share to Lactoferrin

Share to Lipid Metabolism

Share to Lipoprotein Lipase

Share to Lipoproteins, VLDL

Share to Triglycerides

Source

Identifiers

PMID: 15576844
DOI: 10.1194/jlr.M400301-JLR200

Genes

APOC1
LPL

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Severe hypertriglyceridemia in human APOC1 transgenic mice is caused by apoC-I-induced inhibition of LPL.PMID 15576844Read ↗

Apolipoprotein CI causes hypertriglyceridemia independent of the very-low-density lipoprotein receptor and apolipoprotein CIII in mice.Semantic proximity Read ↗

Increased response to cholesterol feeding in apolipoprotein C1-deficient mice.Semantic proximity Read ↗

High density lipoprotein particle size restriction in apolipoprotein A-I(Milano) transgenic mice.Semantic proximity Read ↗

Creation of Apolipoprotein C-II (ApoC-II) Mutant Mice and Correction of Their Hypertriglyceridemia with an ApoC-II Mimetic Peptide.Semantic proximity Read ↗

ABCA1 Promotes the de Novo Biogenesis of Apolipoprotein CIII-Containing HDL Particles in Vivo and Modulates the Severity of Apolipoprotein CIII-Induced HypertriglyceridemiaSemantic proximity Read ↗

A rare gain of function variant of hepatic lipase attenuates hypercholesterolaemia and atherosclerosis in mice via an LDL receptor-independent mechanism.Semantic proximity Read ↗

ApoC-III inhibits clearance of triglyceride-rich lipoproteins through LDL family receptors.Semantic proximity Read ↗

Characterization of a hypertriglyceridemic transgenic miniature pig model expressing human apolipoprotein CIII.Semantic proximity Read ↗

Hypertriglyceridemia as a Result of Human apo <i>CII</i> Gene Expression in Transgenic MiceSemantic proximity Read ↗

Expression of human apolipoprotein A-II in apolipoprotein E-deficient mice induces features of familial combined hyperlipidemia.Semantic proximity Read ↗

Functional lecithin:cholesterol acyltransferase deficiency and high density lipoprotein deficiency in transgenic mice overexpressing human apolipoprotein A-II.Semantic proximity Read ↗

Elevated triglycerides and low HDL cholesterol in transgenic mice expressing human apolipoprotein A-I(Milano).Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.