Evidence mapPaperPMID 9691099Full record

Trial reportThe Journal of clinical investigation1998

Retinoids increase human apo C-III expression at the transcriptional level via the retinoid X receptor. Contribution to the hypertriglyceridemic action of retinoids.

N Vu-Dac, P Gervois, I P Torra, J C Fruchart, V Kosykh, T Kooistra, H M Princen, J Dallongeville, B Staels

Open access · bronzeAbstract readClinical TrialComparative StudyRandomized Controlled Trial
In one paragraph

Trial report in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

  1. Guideline
  2. The Impact of Isotretinoin on Lipid Profile: a Systematic Review.Annals of medicine and surgery (2012) · 2025
    Review
  3. Review
  4. Article
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  11. The role of the retinoid receptor, RAR/RXR heterodimer, in liver physiology.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  12. Article
  13. The role of β-carotene and vitamin A in atherogenesis: Evidences from preclinical and clinical studies.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
    Review
  14. Article
  15. Article
  16. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

N Vu-DacU.325 Institut National de la Santé et de la Recherche Médicale, Département d'Athérosclérose, Institut Pasteur de Lille, 59019 Lille, France.
P Gervois
I P Torra
J C Fruchart
V Kosykh
T Kooistra
H M Princen
J Dallongeville
B Staels
Inserm · FRInstitute of Experimental Cardiology · RUInstitut Pasteur de Lille · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertriglyceridemia is a metabolic complication of retinoid therapy. In this study, we analyzed whether retinoids increase the expression of apo C-III, an antagonist of plasma triglyceride catabolism. In men, isotretinoin treatment (80 mg/d; 5 d) resulted in elevated plasma apo C-III, but not apo E concentrations. In human hepatoma HepG2 cells, retinoids increased apo C-III mRNA and protein production. Transient transfection experiments indicated that retinoids increase apo C-III expression at the transcriptional level. This increased apo C-III transcription is mediated by the retinoid X receptor (RXR), since LG1069 (4-[1-(5,6,7,8-tetrahydro-3,5,5,8, 8-pentamethyl-2-naphtalenyl)ethenyl]benzoic acid), a RXR-specific agonist, but not TTNPB ((E)- 4-[2-(5,6,7,8-tetrahydro-5,5,8, 8-tetramethyl-2-naphtalenyl)propenyl]benzoic acid), a retinoic acid receptor (RAR)-specific agonist, induced apo C-III mRNA in HepG2 cells and primary human hepatocytes. Mutagenesis experiments localized the retinoid responsiveness to a cis-element consisting of two imperfect AGGTCA sequences spaced by one oligonucleotide (DR-1), within the previously identified C3P footprint site. Cotransfection assays showed that RXR, but not RAR, activates apo C-III transcription through this element either as a homo- or as a heterodimer with the peroxisome proliferator-activated receptor. Thus, apo C-III is a target gene for retinoids acting via RXR. Increased apo C-III expression may contribute to the hypertriglyceridemia and atherogenic lipoprotein profile observed after retinoid therapy.

Indexed as

AdultApolipoprotein C-IIIApolipoproteins CBenzoatesBexaroteneCarcinoma, HepatocellularCells, CulturedDimerizationDouble-Blind MethodGene Expression RegulationHeLa CellsHumansHypertriglyceridemiaIsotretinoinLiverLiver Neoplasms4-(2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1-propenyl)benzoic acidApolipoprotein C-IIIApolipoproteins CBenzoatesBexaroteneIsotretinoinReceptors, Cytoplasmic and NuclearReceptors, Retinoic AcidRecombinant Fusion ProteinsRetinoidsRetinoid X ReceptorsTetrahydronaphthalenesTranscription Factors

Identifiers

PMID9691099
PMCPMC508923
OpenAlexW2074626161

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.