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

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

doi:10.1172/jci1581

Cited by 143Lipid metabolism and disordersRetinoids in leukemia and cellular processesPeroxisome Proliferator-Activated Receptors

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

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Vu-Dac, N, Gervois, P, Torra, I P, Fruchart, J C, Kosykh, V, Kooistra, T, Princen, H M, Dallongeville, J +1 more·1998·Journal of Clinical Investigation

DOI 10.1172/jci1581PMC PMC508923

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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.

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Retinoids such as isotretinoin and the anticancer drug bexarotene increase triglyceride levels.
“An increase in hepatic VLDL and apoC-III production and perhaps a decrease in LpL leading to increased triglyceride levels are also seen during use of retinoids such as isotretinoin and the anticancer drug bexarotene (110 -112).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [111]
The isotretinoin-treatment results report a significant increase in plasma triglycerides in nine volunteers. Our copy does not mention bexarotene, so it cannot support that specific example. The Discussion also says isotretinoin did not change postheparin LPL activity, limiting support for the fuller citing sentence’s proposed mechanism. (LLM, conf=0.88)
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Authors: Vu-Dac, N., Gervois, P., Torra, I. P., Fruchart, J. C., Kosykh, V, Kooistra, T., Princen, H. M., Dallongeville, J., & Staels, B.
Affiliations: Inserm (FR)
Université de Lille (FR)
Netherlands Organisation for Applied Scientific Research (NL)
Corresponding author: Staels, B
ORCID: Gervois, P
Staels, B
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1998-08-01
Volume: 102
Issue: 3
Pages: 625-632
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci1581
PMC: PMC508923
OpenAlex: W2074626161
Cited by: 143
References: 67
Citations by year: 2026: 1 · 2025: 5 · 2024: 2 · 2023: 2 · 2022: 5 · 2021: 4 · 2020: 2 · 2019: 7 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 4 · 2014: 7 · 2013: 8 · 2012: 7
FWCI: 5.02
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
TNO Repository (submittedVersion)
UCL Discovery (University College London) (submittedVersion)
Repository hosted by TU Delft Library (TU Delft) (submittedVersion)
Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
Funders: Institut National de la Santé et de la Recherche Médicale
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords: retinoids, apolipoprotein C-III, retinoid X receptor, hypertriglyceridemia, isotretinoin, transcriptional regulation, peroxisome proliferator-activated receptors, retinoic acid receptor, hepatocytes, hepatic gene expression, atherogenic lipoproteins, apolipoprotein E
MeSH terms: Bexarotene, Adult, Apolipoproteins C, Benzoates, Cells, Cultured, Double-Blind Method, Gene Expression Regulation, HeLa Cells, Carcinoma, Hepatocellular, Humans, Liver, Liver Neoplasms, Male, Promoter Regions, Genetic, Recombinant Fusion Proteins, Regulatory Sequences, Nucleic Acid, Retinoids, Tetrahydronaphthalenes, Transcription Factors, Transcription, Genetic, Transfection, Tumor Cells, Cultured, Hypertriglyceridemia, Isotretinoin, Mutagenesis, Site-Directed, Receptors, Cytoplasmic and Nuclear, Receptors, Retinoic Acid, Dimerization, Retinoid X Receptors, Apolipoprotein C-III

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

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