Evidence map›Paper›PMID 23073827›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2012

Fasting-induced FGF21 is repressed by LXR activation via recruitment of an HDAC3 corepressor complex in mice.

Amena Archer, Nicolas Venteclef, Agneta Mode, Matteo Pedrelli, Chiara Gabbi, Karine Clément, Paolo Parini, Jan-Åke Gustafsson, Marion Korach-André

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Mutually exclusive alternative pre-mRNA splicing promotes adaptive metabolic stress signaling by JNK.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  11. Nuclear receptors and nonalcoholic fatty liver disease.Biochimica et biophysica acta · 2016
    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 6 institutions in 3 countries.

Amena ArcherDepartment of Biosciences and Nutrition and Center for Biosciences at Novum, Karolinska Institute, S-141 83 Huddinge, Sweden.
Nicolas Venteclef
Agneta Mode
Matteo Pedrelli
Chiara Gabbi
Karine Clément
Paolo Parini
Jan-Åke Gustafsson
Marion Korach-André
Science for Life Laboratory · SEKarolinska Institutet · SECentre de Recherche des Cordeliers · FRKarolinska University Hospital · SEPitié-Salpêtrière Hospital · FRUniversity of Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver plays a pivotal role in the physiological adaptation to fasting and a better understanding of the metabolic adaptive responses may give hints on new therapeutic strategies to control the metabolic diseases. The liver X receptors (LXRs) are well-established regulators of lipid and glucose metabolism. More recently fibroblast growth factor 21 (FGF21) has emerged as an important regulator of energy homeostasis. We hypothesized that the LXR transcription factors could influence Fgf21 expression, which is induced in response to fasting. Wild-type, LXRα(-/-), and LXRβ(-/-) mice were treated for 3 d with vehicle or the LXR agonist GW3965 and fasted for 12 h prior to the killing of the animals. Interestingly, serum FGF21 levels were induced after fasting, but this increase was blunted when the mice were treated with GW3965 independently of genotypes. Compared with wild-type mice, GW3965-treated LXRα(-/-) and LXRβ(-/-) mice showed improved insulin sensitivity and enhanced ketogenic response at fasting. Of note is that during fasting, GW3965 treatment tended to reduce liver triglycerides as opposed to the effect of the agonist in the fed state. The LXR-dependent repression of Fgf21 seems to be mainly mediated by the recruitment of LXRβ onto the Fgf21 promoter upon GW3965 treatment. This repression by LXRβ occurs through the recruitment and stabilization of the repressor complex composed of retinoid-related orphan receptor-α/Rev-Erbα/histone deacetylase 3 onto the Fgf21 promoter. Our data clearly demonstrate that there is a cross talk between the LXR and FGF21 signaling pathways in the adaptive response to fasting.

Indexed as

AnimalsBenzoatesBenzylaminesFastingFibroblast Growth FactorsGlucoseHistone Deacetylase 3Histone DeacetylasesHomeostasisInsulin ResistanceLipid MetabolismLiverLiver X ReceptorsMaleMiceMice, Inbred C57BLBenzoatesBenzylaminesfibroblast growth factor 21Fibroblast Growth FactorsGlucoseGW 3965Histone Deacetylase 3Histone DeacetylasesLiver X ReceptorsNr1d1 protein, mouseNr1h3 protein, mouseNuclear Receptor Subfamily 1, Group D, Member 1Nuclear Receptor Subfamily 1, Group F, Member 1Orphan Nuclear ReceptorsTriglycerides

Identifiers

PMID23073827
PMCPMC5416953
OpenAlexW2049567594

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.