ArticleThe Journal of clinical investigation1995
Common genetic variation in the promoter of the human apo CIII gene abolishes regulation by insulin and may contribute to hypertriglyceridemia.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 3 of them syntheses that pooled it.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
81 citing papers in PubMed, 3 syntheses or guidelines pooled it, 281 citations in OpenAlex.
- A PRISMA-compliant meta-analysis of apolipoprotein C3 polymorphisms and nonalcoholic fatty liver disease.Journal of the Chinese Medical Association : JCMA · 2021Pooled it
- Association between APOC3 polymorphisms and non-alcoholic fatty liver disease risk: a meta-analysis.African health sciences · 2020Pooled it
- Association of the polymorphisms of the genes APOC3 (rs2854116), ESR2 (rs3020450), HFE (rs1799945), MMP1 (rs1799750) and PPARG (rs1801282) with lipodystrophy in people living with HIV on antiretroviral therapy: a systematic review.Molecular biology reports · 2020Pooled it
- Trial
- 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
- Olezarsen and Beyond: Emerging Targeted Treatments for Familial Chylomicronemia Syndrome and Related Triglyceride Disorders.Journal of lipid and atherosclerosis · 2026Review
- Association of Apolipoprotein C-III Gene Polymorphisms (rs2854116 and rs2854117) with Susceptibility to Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in a Turkish Population.Medicina (Kaunas, Lithuania) · 2025Article
- Metabolic syndrome and effect of gene polymorphisms: ADIPOQ, AGT, AGTR1, AGTR2, ApoC-III, NR3C1 and GNB3 gene polymorphisms.Molecular biology reports · 2025Article
- Article
- Article
- Exploring apolipoprotein C-III: pathophysiological and pharmacological relevance.Cardiovascular research · 2024Review
- Advances in Dyslipidaemia Treatments: Focusing on ApoC3 and ANGPTL3 Inhibitors.Journal of lipid and atherosclerosis · 2024Review
- Insulin Regulation of Hepatic Lipid Homeostasis.Comprehensive Physiology · 2023Review
- Nutrigenetic Interaction Between Apolipoprotein C3 Polymorphism and Fat Intake in People with Nonalcoholic Fatty Liver Disease.Current developments in nutrition · 2023Article
- SNPs in apolipoproteins contribute to sex-dependent differences in blood lipids before and after a high-fat dietary challenge in healthy U.S. adults.BMC nutrition · 2022Article
- Apolipoprotein C-III predicts cardiovascular events and mortality in individuals with type 1 diabetes and albuminuria.Journal of internal medicine · 2022Observational
- Apolipoprotein CIII Is an Important Piece in the Type-1 Diabetes Jigsaw Puzzle.International journal of molecular sciences · 2021Review
- Apolipoprotein C-III and cardiovascular diseases: when genetics meet molecular pathologies.Molecular biology reports · 2021Review
- Apolipoprotein CIII predicts cardiovascular events in patients with coronary artery disease: a prospective observational study.Lipids in health and disease · 2020Observational
- Assessment of Genetic Aspects of Non-alcoholic Fatty Liver and Premature Cardiovascular Events.Middle East journal of digestive diseases · 2020Review
21 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Overexpression of plasma apolipoprotein CIII (apo CIII) causes hypertriglyceridemia in transgenic mice. A genetically variant form of the human apo CIII promoter, containing five single base pair changes, has been shown to be associated with severe hypertriglyceridemia in a patient population. In animals and in cultured cells the apo CIII gene is transcriptionally downregulated by insulin. In this study we demonstrate that, unlike the wild-type promoter, the variant promoter was defective in its response to insulin treatment, remaining constitutively active at all concentrations of insulin. The loss of insulin regulation was mapped to polymorphic sites at -482 and -455, which fall within a previously identified insulin response element. Loss of insulin regulation could result in overexpression of the apo CIII gene and contribute to the development of hypertriglyceridemia. The variant apo CIII promoter is common in the human population and may represent a major contributing factor to the development of hypertriglyceridemia.
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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 Socratic graph.