Evidence map›Paper›PMID 16184193›Full record

ArticleThe Journal of clinical investigation2005

Polyunsaturated fatty acids suppress glycolytic and lipogenic genes through the inhibition of ChREBP nuclear protein translocation.

Renaud Dentin, Fadila Benhamed, Jean-Paul Pégorier, Fabienne Foufelle, Benoit Viollet, Sophie Vaulont, Jean Girard, Catherine Postic

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 1 pooled it
14.9field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 1 synthesis or guideline pooled it, 313 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Triglycerides, Glucose Metabolism, and Type 2 Diabetes.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Response of Primary Human Adipocytes to Fatty Acid Treatment.Journal of cellular and molecular medicine · 2025
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

65 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

Renaud DentinDépartement d'Endocrinologie, Institut Cochin, INSERM U567 CNRS UMR8104, Université René Descartes, Paris, France.
Fadila Benhamed
Jean-Paul Pégorier
Fabienne Foufelle
Benoit Viollet
Sophie Vaulont
Jean Girard
Catherine Postic
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dietary polyunsaturated fatty acids (PUFAs) are potent inhibitors of hepatic glycolysis and lipogenesis. Recently, carbohydrate-responsive element-binding protein (ChREBP) was implicated in the regulation by glucose of glycolytic and lipogenic genes, including those encoding L-pyruvate kinase (L-PK) and fatty acid synthase (FAS). The aim of our study was to assess the role of ChREBP in the control of L-PK and FAS gene expression by PUFAs. We demonstrated in mice, both in vivo and in vitro, that PUFAs [linoleate (C18:2), eicosapentanoic acid (C20:5), and docosahexaenoic acid (C22:6)] suppressed ChREBP activity by increasing ChREBP mRNA decay and by altering ChREBP translocation from the cytosol to the nucleus, independently of an activation of the AMP-activated protein kinase, previously shown to regulate ChREBP activity. In contrast, saturated [stearate (C18)] and monounsaturated fatty acids [oleate (C18:1)] had no effect. Since glucose metabolism via the pentose phosphate pathway is determinant for ChREBP nuclear translocation, the decrease in xylulose 5-phosphate concentrations caused by a PUFA diet favors a PUFA-mediated inhibition of ChREBP translocation. In addition, overexpression of a constitutive nuclear ChREBP isoform in cultured hepatocytes significantly reduced the PUFA inhibition of both L-PK and FAS gene expression. Our results demonstrate that the suppressive effect of PUFAs on these genes is primarily caused by an alteration of ChREBP nuclear translocation. In conclusion, we describe a novel mechanism to explain the inhibitory effect of PUFAs on the genes encoding L-PK and FAS and demonstrate that ChREBP is a pivotal transcription factor responsible for coordinating the PUFA suppression of glycolytic and lipogenic genes.

Indexed as

AMP-Activated Protein KinasesAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCells, CulturedDietary Fats, UnsaturatedDocosahexaenoic AcidsDown-RegulationEicosapentaenoic AcidFatty Acid SynthasesGene Expression Regulation, EnzymologicGlycolysisHepatocytesLipogenesisMaleMiceMultienzyme ComplexesAMP-Activated Protein KinasesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsDietary Fats, UnsaturatedDocosahexaenoic AcidsEicosapentaenoic AcidFatty Acid SynthasesMlxipl protein, mouseMultienzyme ComplexesNuclear ProteinsProtein Serine-Threonine KinasesPyruvate KinaseTranscription Factors

Identifiers

PMID16184193
PMCPMC1224299
OpenAlexW2114472618

What OpenQuestion 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 OpenQuestion graph.