Trial reportJCI insight2022
Postprandial metabolism of apolipoproteins B48, B100, C-III, and E in humans with APOC3 loss-of-function mutations.
Trial report in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Fructose Consumption Aggravates Dysregulation of Postprandial Lipid Metabolism in Obese Hypertriglyceridemic Men With High Cardiometabolic Risk Profile and Associates With Liver Fat Deposition
Genetic Regulation of Lipid Pathways Contributing to Non-alcoholic Fatty Liver and Atherogenic Dyslipidemia
Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Trial
- The FGF21 analog pegozafermin in severe hypertriglyceridemia: a randomized phase 2 trial.Nature medicine · 2023Trial
- Angiopoietin-like protein 3 complete and partial deficiency markedly accelerates apolipoprotein B48 and B100 metabolism in triglyceride-rich lipoproteins in humans.Journal of internal medicine · 2026Article
- Apolipoprotein C-III: Risk-factor, Regulator of Triglyceride-rich Lipoprotein Metabolism and Therapeutic Target.Current atherosclerosis reports · 2026Review
- Exploratory whole-exome analysis of low-density lipoprotein cholesterol and triglyceride response to Mediterranean-style dietary guidance: a focus on plasma lipoprotein pathways.Frontiers in nutrition · 2026Article
- Clinical staging to guide management of metabolic disorders and their sequelae: a European Atherosclerosis Society consensus statement.European heart journal · 2025Article
- Novel Therapeutics for Familial Chylomicronemia Syndrome.Current atherosclerosis reports · 2025Review
- Remnant cholesterol concentrations best explain the cardiovascular benefit of APOC3 genetic inhibition: a drug target Mendelian randomization study.European heart journal open · 2025Article
- Exploring apolipoprotein C-III: pathophysiological and pharmacological relevance.Cardiovascular research · 2024Review
- Apolipoprotein C3: form begets function.Journal of lipid research · 2024Review
- Novel and future lipid-modulating therapies for the prevention of cardiovascular disease.Nature reviews. Cardiology · 2023Review
- Sugar and Dyslipidemia: A Double-Hit, Perfect Storm.Journal of clinical medicine · 2023Review
- Quartet of APOCs and the Different Roles They Play in Diabetes.Arteriosclerosis, thrombosis, and vascular biology · 2023Review
- Triglyceride-Rich Lipoprotein Metabolism: Key Regulators of Their Flux.Journal of clinical medicine · 2023Review
- Broadening the Scope of Dyslipidemia Therapy by Targeting APOC3 (Apolipoprotein C3) and ANGPTL3 (Angiopoietin-Like Protein 3).Arteriosclerosis, thrombosis, and vascular biology · 2023Review
- The chylomicron saga: time to focus on postprandial metabolism.Frontiers in endocrinology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BackgroundApolipoprotein C-III (apoC-III) is a regulator of triglyceride (TG) metabolism, and due to its association with risk of cardiovascular disease, is an emergent target for pharmacological intervention. The impact of substantially lowering apoC-III on lipoprotein metabolism is not clear.MethodsWe investigated the kinetics of apolipoproteins B48 and B100 (apoB48 and apoB100) in chylomicrons, VLDL1, VLDL2, IDL, and LDL in patients heterozygous for a loss-of-function (LOF) mutation in the APOC3 gene. Studies were conducted in the postprandial state to provide a more comprehensive view of the influence of this protein on TG transport.ResultsCompared with non-LOF variant participants, a genetically determined decrease in apoC-III resulted in marked acceleration of lipolysis of TG-rich lipoproteins (TRLs), increased removal of VLDL remnants from the bloodstream, and substantial decrease in circulating levels of VLDL1, VLDL2, and IDL particles. Production rates for apoB48-containing chylomicrons and apoB100-containing VLDL1 and VLDL2 were not different between LOF carriers and noncarriers. Likewise, the rate of production of LDL was not affected by the lower apoC-III level, nor were the concentration and clearance rate of LDL-apoB100.ConclusionThese findings indicate that apoC-III lowering will have a marked effect on TRL and remnant metabolism, with possibly significant consequences for cardiovascular disease prevention.Trial registrationClinicalTrials.gov NCT04209816 and NCT01445730.FundingSwedish Heart-Lung Foundation, Swedish Research Council, ALF grant from the Sahlgrenska University Hospital, Novo Nordisk Foundation, Sigrid Juselius Foundation, Helsinki University Hospital Government Research funds, Finnish Heart Foundation, and Finnish Diabetes Research Foundation.
Indexed as
Identifiers
What Socratic holds
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.