Evidence map›Paper›PMID 42762974›Full record

ArticleMolecular metabolism2026

Pregnane X receptor deletion induces a lean phenotype in chow-fed mice through a liver-ileum-muscle axis involving 6α-hydroxylated bile acids and Fgf15.

Bérengère Benoit, Audrey Jalabert, Emmanuelle Meugnier, Stéphanie Chanon, Aurélie Vieille-Marchiset, Alice Beau, Sandra Pesenti, Emmanuelle Loizon, Oriane Vitalis, Nadia Bendridi and 9 more

Abstract read
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In one paragraph

Article in Molecular metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Bérengère BenoitUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France. Electronic address: Berengere.benoit@univ-lyon1.fr.
Audrey JalabertUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Emmanuelle MeugnierUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Stéphanie ChanonUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Aurélie Vieille-MarchisetUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Alice BeauUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Sandra PesentiUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Emmanuelle LoizonUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Oriane VitalisUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France; Metanutribiota platform, Centre de Biologie et de Pathologie, Hospices Civils de Lyon, Groupement Hospitalier Sud, Pierre Bénite, France.
Nadia BendridiUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Margaux NawrotUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Kassem MakkiUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Brigitte Le Magueresse-BattistoniUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Jennifer RieussetUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Marie-Caroline MichalskiUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Dominique RainteauSorbonne Université, Saint Antoine Research Center, INSERM UMR 938, Département de Métabolomique Clinique, Hôpital Saint Antoine, AP-HP Sorbonne Université, Paris, France.
Karim ChikhUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France; Metanutribiota platform, Centre de Biologie et de Pathologie, Hospices Civils de Lyon, Groupement Hospitalier Sud, Pierre Bénite, France.
Hubert VidalUniversité Lyon1, CarMeN Laboratory, INSERM, INRAE, Pierre Bénite, France.
Jérôme RuzzinDepartment of Biology, University of Bergen, Bergen, Norway; Department of Molecular Medicine, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe pregnane X receptor (Pxr; Nr1i2) plays a role in metabolic regulation. However, its contribution to systemic energy homeostasis under physiological conditions remains unclear. Here, we investigated the metabolic consequences of Nr1i2 deficiency in chow-fed mice.

methodsPhenotyping was performed in adult whole-body Nr1i2 knockout (Nr1i2

resultsChow-fed Nr1i2

conclusionsThese findings provide the first evidence that, under standard dietary conditions, loss of Pxr induces a lean phenotype, promotes reduced adiposity together with remodeling of bile acid pool, increased Fgf15 production and enhanced skeletal muscle mass.

Indexed as

Bile acidsEnergy metabolismFGF15/19Pregnane X receptor (PXR/NR1I2)Skeletal muscle

Identifiers

PMID42762974

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Registered trials

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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.