Evidence map›Paper›PMID 21464203›Full record

ArticleJournal of lipid research2011

Studies in mice, hamsters, and rats demonstrate that repression of hepatic apoA-I expression by taurocholic acid in mice is not mediated by the farnesoid-X-receptor.

Christophe Gardès, Denise Blum, Konrad Bleicher, Evelyne Chaput, Martin Ebeling, Peter Hartman, Corinne Handschin, Hans Richter, G Martin Benson

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  6. Nuclear bile acid signaling through the farnesoid X receptor.Cellular and molecular life sciences : CMLS · 2015
    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 1 institution in 1 country.

Christophe GardèsDepartments of Metabolic Diseases, F. Hoffmann-La Roche AG, 4070 Basel, Switzerland. Electronic address: christophe.gardes@roche.com.
Denise BlumDepartments of Metabolic Diseases, F. Hoffmann-La Roche AG, 4070 Basel, Switzerland.
Konrad BleicherChemistry, F. Hoffmann-La Roche AG, 4070 Basel, Switzerland.
Evelyne ChaputDepartments of Metabolic Diseases, F. Hoffmann-La Roche AG, 4070 Basel, Switzerland.
Martin EbelingBio-informatics, F. Hoffmann-La Roche AG, 4070 Basel, Switzerland.
Peter HartmanDepartments of Metabolic Diseases, F. Hoffmann-La Roche AG, 4070 Basel, Switzerland.
Corinne HandschinDepartments of Metabolic Diseases, F. Hoffmann-La Roche AG, 4070 Basel, Switzerland.
Hans RichterChemistry, F. Hoffmann-La Roche AG, 4070 Basel, Switzerland.
G Martin BensonDepartments of Metabolic Diseases, F. Hoffmann-La Roche AG, 4070 Basel, Switzerland.
Roche (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is claimed that apoA-I expression is repressed in mice by cholic acid (CA) and its taurine conjugate, taurocholic acid (TCA) via farnesoid X receptor (FXR) activation. We measured apoA-I expression in mice, hamsters, and rats treated with highly potent and selective synthetic FXR agonists or with TCA. All of the synthetic agonists bound to FXR with high affinity in a scintillation proximity assay. However, TCA did not compete with the radioligand up to the highest concentration used (100 μM). The C-site regulatory region of apoA-I, through which FXR has been reported to regulate its expression, is completely conserved across the species investigated. In both male and female human apoA-I-transgenic mice, we reproduced the previously reported strong inhibition of human apoA-I expression upon treatment with the typical supraphysiological dose of TCA used in such studies. However, in contrast to some previous reports, TCA did not repress murine apoA-I expression in the same mice. Also, more-potent and -selective FXR agonists did not affect human or murine apoA-I expression in this model. In LDL receptor-deficient mice and Golden Syrian hamsters, selective FXR agonists did not affect apoA-I expression, whereas in Wistar rats, some even increased apoA-I expression. In conclusion, selective FXR agonists do not repress apoA-I expression in rodents. Repression of human apoA-I expression by TCA in transgenic mice is probably mediated through FXR-independent mechanisms.

Indexed as

Apolipoprotein A-IAnimalsBinding SitesConserved SequenceCricetinaeFemaleGene Expression RegulationHumansLiverMaleMesocricetusMiceMice, Inbred C57BLMice, TransgenicPromoter Regions, GeneticProtein BindingApolipoprotein A-IReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearRNA, MessengerTaurocholic Acid

Identifiers

PMID21464203
PMCPMC3090240
OpenAlexW2083034596

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.