Evidence map›Paper›PMID 35041621›Full record

ArticleJCI insight2022

ChREBPβ is dispensable for the control of glucose homeostasis and energy balance.

Emeline Recazens, Geneviève Tavernier, Jérémy Dufau, Camille Bergoglio, Fadila Benhamed, Stéphanie Cassant-Sourdy, Marie-Adeline Marques, Sylvie Caspar-Bauguil, Alice Brion, Laurent Monbrun and 9 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Insulin Deficiency Exacerbates Muscle Atrophy and Osteopenia inInternational journal of molecular sciences · 2025
    Article
  2. Role of ChREBP-PPARα-FGF21 Axis in Metabolic Dysfunction of MASLD.International journal of molecular sciences · 2025
    Article
  3. Review
  4. Review
  5. Review
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

19 authors at 2 institutions in 1 country.

Emeline RecazensInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Geneviève TavernierInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Jérémy DufauInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Camille BergoglioInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Fadila BenhamedUniversity of Paris, Cochin Institute, CNRS, INSERM, Paris, France.
Stéphanie Cassant-SourdyInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Marie-Adeline MarquesInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Sylvie Caspar-BauguilInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Alice BrionGenome Structure and Instability Laboratory, INSERM, CNRS, National Museum of Natural History, Paris, France.
Laurent MonbrunInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Renaud DentinUniversity of Paris, Cochin Institute, CNRS, INSERM, Paris, France.
Clara FerrierInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Mélanie LerouxInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Pierre-Damien DenechaudInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Cedric MoroInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Jean-Paul ConcordetGenome Structure and Instability Laboratory, INSERM, CNRS, National Museum of Natural History, Paris, France.
Catherine PosticUniversity of Paris, Cochin Institute, CNRS, INSERM, Paris, France.
Etienne MouiselInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Dominique LanginInstitute of Metabolic and Cardiovascular Diseases (I2MC), Equipe MetaDiab, University of Toulouse, INSERM, University of Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Université Toulouse III - Paul Sabatier · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impaired glucose metabolism is observed in obesity and type 2 diabetes. Glucose controls gene expression through the transcription factor ChREBP in liver and adipose tissues. Mlxipl encodes 2 isoforms: ChREBPα, the full-length form (translocation into the nucleus is under the control of glucose), and ChREBPβ, a constitutively nuclear shorter form. ChREBPβ gene expression in white adipose tissue is strongly associated with insulin sensitivity. Here, we investigated the consequences of ChREBPβ deficiency on insulin action and energy balance. ChREBPβ-deficient male and female C57BL6/J and FVB/N mice were produced using CRISPR/Cas9-mediated gene editing. Unlike global ChREBP deficiency, lack of ChREBPβ showed modest effects on gene expression in adipose tissues and the liver, with variations chiefly observed in brown adipose tissue. In mice fed chow and 2 types of high-fat diets, lack of ChREBPβ had moderate effects on body composition and insulin sensitivity. At thermoneutrality, ChREBPβ deficiency did not prevent the whitening of brown adipose tissue previously reported in total ChREBP-KO mice. These findings revealed that ChREBPβ is dispensable for metabolic adaptations to nutritional and thermic challenges.

Indexed as

Diabetes Mellitus, ExperimentalGene Expression RegulationAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBlood GlucoseCells, CulturedDiabetes Mellitus, Type 2Energy MetabolismFemaleMaleMiceMice, Inbred C57BLRNABasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBlood GlucoseMlxipl protein, mouseRNAAdipose tissueCarbohydrate metabolismMetabolismObesity

Identifiers

PMID35041621
PMCPMC8876429
OpenAlexW4205111778

What OpenQuestion holds

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LicenceCC BY
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.