Evidence map›Paper›PMID 25061560›Full record

ArticleMolecular metabolism2014

11β-Hydroxysteroid dehydrogenase-1 is involved in bile acid homeostasis by modulating fatty acid transport protein-5 in the liver of mice.

Carlos A Penno, Stuart A Morgan, Adam J Rose, Stephan Herzig, Gareth G Lavery, Alex Odermatt

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2014. 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
0.4field-weighted citation impact, top 32% 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, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
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

6 authors at 3 institutions in 3 countries.

Carlos A PennoDivision of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Klingelbergstrasse 50, 4056 Basel, Switzerland.
Stuart A MorganCentre for Endocrinology Diabetes and Metabolism (CEDAM), Institute of Biomedical Research, Medical School Building, School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Adam J RoseJoint Research Division, Molecular Metabolic Control, German Cancer Research Center (DKFZ) Heidelberg, Center for Molecular Biology (ZMBH), Heidelberg University, Network Aging Research, University Hospital Heidelberg, Germany.
Stephan HerzigJoint Research Division, Molecular Metabolic Control, German Cancer Research Center (DKFZ) Heidelberg, Center for Molecular Biology (ZMBH), Heidelberg University, Network Aging Research, University Hospital Heidelberg, Germany.
Gareth G LaveryCentre for Endocrinology Diabetes and Metabolism (CEDAM), Institute of Biomedical Research, Medical School Building, School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Alex OdermattDivision of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Klingelbergstrasse 50, 4056 Basel, Switzerland.
German Cancer Research Center · DEUniversity of Basel · CHUniversity of Birmingham · GB

Funding

Biotechnology and Biological Sciences Research Council BB/G023468/1Medical Research Council MR/K00414X/1
6 · The paper itself

Abstract

11β-Hydroxysteroid dehydrogenase-1 (11β-HSD1) plays a key role in glucocorticoid receptor (GR) activation. Besides, it metabolizes some oxysterols and bile acids (BAs). The GR regulates BA homeostasis; however, the impact of impaired 11β-HSD1 activity remained unknown. We profiled plasma and liver BAs in liver-specific and global 11β-HSD1-deficient mice. 11β-HSD1-deficiency resulted in elevated circulating unconjugated BAs, an effect more pronounced in global than liver-specific knockout mice. Gene expression analyses revealed decreased expression of the BA-CoA ligase Fatp5, suggesting impaired BA amidation. Reduced organic anion-transporting polypeptide-1A1 (Oatp1a1) and enhanced organic solute-transporter-β (Ostb) mRNA expression were observed in livers from global 11β-HSD1-deficient mice. The impact of 11β-HSD1-deficiency on BA homeostasis seems to be GR-independent because intrahepatic corticosterone and GR target gene expression were not substantially decreased in livers from global knockout mice. Moreover, Fatp5 expression in livers from hepatocyte-specific GR knockout mice was unchanged. The results revealed a role for 11β-HSD1 in BA homeostasis.

Indexed as

11β-Hydroxysteroid dehydrogenase11β-hydroxysteroid dehydrogenase 1, 11β-HSD1BA coenzyme A: amino acid N-acyltransferase, BaatBile acid conjugationBile acidsbile acids, BAsBile acid transportcholesterol 7α-hydroxylase, Cyp7a1farnesoid X receptor, Fxrfatty acid transport protein, Fatpglucocorticoid receptor, GRGlucocorticoidsNa+-taurocholate cotransporting polypeptide, NtcpOrganic anion-transporting polypeptide, OatpOrganic solute transporter, Ostshort heterodimer partner, Shpsterol-regulatory element-binding protein 1C, Srebp1c

Identifiers

PMID25061560
PMCPMC4099504
OpenAlexW2164351256

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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.