ArticleThe Journal of clinical investigation1997
Chylomicronemia due to apolipoprotein CIII overexpression in apolipoprotein E-null mice. Apolipoprotein CIII-induced hypertriglyceridemia is not mediated by effects on apolipoprotein E.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 189 citations in OpenAlex.
- Evinacumab in severe hypertriglyceridemia with or without lipoprotein lipase pathway mutations: a phase 2 randomized trial.Nature medicine · 2023Trial
- Retinoids increase human apo C-III expression at the transcriptional level via the retinoid X receptor. Contribution to the hypertriglyceridemic action of retinoids.The Journal of clinical investigation · 1998Trial
- Cardiac Lipid Metabolism: Cells, Metabolites, and Rhythms.Circulation research · 2026Review
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- Moderate-intensity continuous training reduces triglyceridemia and improves oxygen consumption in dyslipidemic apoCIII transgenic mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- Increased atherosclerosis in a mouse model of glycogen storage disease type 1a.Molecular genetics and metabolism reports · 2022Article
- Genetically-engineered hamster models: applications and perspective in dyslipidemia and atherosclerosis-related cardiovascular disease.Medical review (2021) · 2021Article
- Apolipoprotein CIII Is an Important Piece in the Type-1 Diabetes Jigsaw Puzzle.International journal of molecular sciences · 2021Review
- Lipoprotein Lipase and Its Regulators: An Unfolding Story.Trends in endocrinology and metabolism: TEM · 2021Review
- Apolipoprotein CIII Deficiency Protects Against Atherosclerosis in Knockout Rabbits.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Adropin as A Fat-Burning Hormone with Multiple Functions-Review of a Decade of Research.Molecules (Basel, Switzerland) · 2020Review
- Potential osteomyelitis biomarkers identified by plasma metabolome analysis in mice.Scientific reports · 2020Article
- The Roles of ApoC-III on the Metabolism of Triglyceride-Rich Lipoproteins in Humans.Frontiers in endocrinology · 2020Review
- ApoC-III ASO promotes tissue LPL activity in the absence of apoE-mediated TRL clearance.Journal of lipid research · 2019Article
- Emerging Evidence that ApoC-III Inhibitors Provide Novel Options to Reduce the Residual CVD.Current atherosclerosis reports · 2019Review
- Apolipoprotein C-III inhibits triglyceride hydrolysis by GPIHBP1-bound LPL.Journal of lipid research · 2017Article
- Pleiotropic effects of apolipoprotein C3 on HDL functionality and adipose tissue metabolic activity.Journal of lipid research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism of apolipoprotein (apo) CIII-induced hypertriglyceridemia remains uncertain. We crossed apoCIII transgenic and apoE gene knockout (apoE0) mice, and observed severe hypertriglyceridemia with plasma triglyceride levels of 4,521+/-6, 394 mg/dl vs. 423+/-106 mg/dl in apoE0 mice, P < 0.00001 for log(triglycerides [TG]). Cholesterols were 1,181+/-487 mg/dl vs. 658+/-151 mg/dl, P < 0.0001. Lipoprotein fractionation showed a marked increase in triglyceride-enriched chylomicrons+VLDL. This increase was limited to the lowest density (chylomicrons and Sf 100-400) subfractions. Intermediate density lipoproteins (IDL)+LDL increased moderately, and HDL decreased. There was no significant increase in triglyceride production in apoCIII transgenic/apoE0 mice. The clearance of VLDL triglycerides, however, was significantly decreased. Lipoprotein lipase in postheparin plasma was elevated, but activation studies suggested LPL inhibition by both apoCIII transgenic and apoCIII transgenic/apoE0 plasma. ApoCIII overexpression also produced a marked decrease in VLDL glycosaminoglycan binding which was independent of apoE. The predominant mechanism of apoCIII-induced hypertriglyceridemia appears to be decreased lipolysis at the cell surface. The altered lipoprotein profile that was produced also allowed us to address the question of the direct atherogenicity of chylomicrons and large VLDL. Quantitative arteriosclerosis studies showed identical results in both apoCIII transgenic/apoE0 and apoE0 mice, supporting the view that very large triglyceride-enriched particles are not directly atherogenic.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.