Evidence map›Paper›PMID 28315136›Full record

ArticleLipids2017

Ursodeoxycholic Acid Suppresses Lipogenesis in Mouse Liver: Possible Role of the Decrease in β-Muricholic Acid, a Farnesoid X Receptor Antagonist.

Kyosuke Fujita, Yusuke Iguchi, Mizuho Une, Shiro Watanabe

Abstract read
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In one paragraph

Article in Lipids, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  7. Impacts of liver macrophages, gut microbiota, and bile acid metabolism on the differences in iHFC diet-induced MASH progression between TSNO and TSOD mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  8. Characterization of individual bile acids in vivo utilizing a novel low bile acid mouse model.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Article
  9. Review
  10. 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

4 authors at 2 institutions in 2 countries.

Kyosuke FujitaDivision of Nutritional Biochemistry, Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Yusuke IguchiFaculty of Pharmaceutical Science, Hiroshima International University, Kure, Hiroshima, 737-0112, Japan.
Mizuho UneFaculty of Pharmaceutical Science, Hiroshima International University, Kure, Hiroshima, 737-0112, Japan.
Shiro WatanabeDivision of Nutritional Biochemistry, Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan. shirowat@inm.u-toyama.ac.jp.
Hiroshima International University · JPUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The farnesoid X receptor (FXR) is a major nuclear receptor of bile acids; its activation suppresses sterol regulatory element-binding protein 1c (SREBP1c)-mediated lipogenesis and decreases the lipid contents in the liver. There are many reports showing that the administration of ursodeoxycholic acid (UDCA) suppresses lipogenesis and reduces the lipid contents in the liver of experimental animals. Since UDCA is not recognized as an FXR agonist, these effects of UDCA cannot be readily explained by its direct activation of FXR. We observed that the dietary administration of UDCA in mice decreased the expression levels of SREBP1c and its target lipogenic genes. Alpha- and β-muricholic acids (MCA) and cholic acid (CA) were the major bile acids in the mouse liver but their contents decreased upon UDCA administration. The hepatic contents of chenodeoxycholic acid and deoxycholic acid (DCA) were relatively low but were not changed by UDCA. UDCA did not show FXR agonistic or antagonistic potency in in vitro FXR transactivation assay. Taking these together, we deduced that the above-mentioned change in hepatic bile acid composition induced upon UDCA administration might cause the relative increase in the FXR activity in the liver, mainly by the reduction in the content of β-MCA, a farnesoid X receptor antagonist, which suggests a mechanism by which UDCA suppresses lipogenesis and decreases the lipid contents in the mouse liver.

Indexed as

AnimalsCell LineChenodeoxycholic AcidCholic AcidsDeoxycholic AcidGene Expression RegulationLipogenesisLiverMaleMiceReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearSterol Regulatory Element Binding Protein 1Ursodeoxycholic AcidChenodeoxycholic AcidCholic AcidsDeoxycholic Acidmuricholic acidReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearSrebf1 protein, mouseSterol Regulatory Element Binding Protein 1Ursodeoxycholic AcidCholesterol esterFatty acidSterol regulatory element-binding protein 1cTriglyceride

Identifiers

PMID28315136
OpenAlexW2596817657

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.