Evidence map›Paper›PMID 29656109›Full record

ArticleMolecular metabolism2018

Bile acids are important direct and indirect regulators of the secretion of appetite- and metabolism-regulating hormones from the gut and pancreas.

Rune E Kuhre, Nicolai J Wewer Albrechtsen, Olav Larsen, Sara L Jepsen, Emilie Balk-Møller, Daniel B Andersen, Carolyn F Deacon, Kristina Schoonjans, Frank Reimann, Fiona M Gribble and 4 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 1% 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

124 citing papers in PubMed, 1 synthesis or guideline pooled it, 217 citations in OpenAlex.

  1. Pooled it
  2. DuodenalGut · 2022
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64 more citing papers are in PubMed but not listed here.

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

14 authors at 3 institutions in 3 countries.

Rune E KuhreDepartment of Biomedical Sciences, University of Copenhagen, DK-2200, Copenhagen, Denmark; NNF Center for Basic Metabolic Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.
Nicolai J Wewer AlbrechtsenDepartment of Biomedical Sciences, University of Copenhagen, DK-2200, Copenhagen, Denmark; NNF Center for Basic Metabolic Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.
Olav LarsenDepartment of Biomedical Sciences, University of Copenhagen, DK-2200, Copenhagen, Denmark.
Sara L JepsenDepartment of Biomedical Sciences, University of Copenhagen, DK-2200, Copenhagen, Denmark; NNF Center for Basic Metabolic Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.
Emilie Balk-MøllerDepartment of Biomedical Sciences, University of Copenhagen, DK-2200, Copenhagen, Denmark; NNF Center for Basic Metabolic Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.
Daniel B AndersenDepartment of Biomedical Sciences, University of Copenhagen, DK-2200, Copenhagen, Denmark; NNF Center for Basic Metabolic Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.
Carolyn F DeaconDepartment of Biomedical Sciences, University of Copenhagen, DK-2200, Copenhagen, Denmark; NNF Center for Basic Metabolic Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.
Kristina SchoonjansLaboratory of Metabolic Signaling, Ecole Polytechnique Fédérale de Lausanne, Station 15, CH-1015, Lausanne, Switzerland.
Frank ReimannMetabolic Research Laboratories and Medical Research Council Metabolic Diseases Unit, Wellcome Trust-Medical Research Council, Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, CB2 0QQ, United Kingdom.
Fiona M GribbleMetabolic Research Laboratories and Medical Research Council Metabolic Diseases Unit, Wellcome Trust-Medical Research Council, Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, CB2 0QQ, United Kingdom.
Reidar AlbrechtsenDepartment of Biomedical Sciences, and Biotech Research and Innovation Centre (BRIC), University of Copenhagen, DK-2200, Copenhagen, Denmark.
Bolette HartmannDepartment of Biomedical Sciences, University of Copenhagen, DK-2200, Copenhagen, Denmark; NNF Center for Basic Metabolic Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.
Mette M RosenkildeDepartment of Biomedical Sciences, University of Copenhagen, DK-2200, Copenhagen, Denmark.
Jens J HolstDepartment of Biomedical Sciences, University of Copenhagen, DK-2200, Copenhagen, Denmark; NNF Center for Basic Metabolic Research, University of Copenhagen, DK-2200, Copenhagen, Denmark. Electronic address: jjholst@sund.ku.dk.
University of Copenhagen · DKAddenbrooke's Hospital · GBÉcole Polytechnique Fédérale de Lausanne · CH

Funding

Medical Research Council MC_UU_00014/3Medical Research Council MC_UU_00014/5Medical Research Council MC_UU_12012/3Medical Research Council MRC_MC_UU_12012/3Wellcome Trust WT106262/Z/14/ZWellcome Trust WT106263/Z/14/Z
6 · The paper itself

Abstract

objectiveBile acids (BAs) facilitate fat absorption and may play a role in glucose and metabolism regulation, stimulating the secretion of gut hormones. The relative importance and mechanisms involved in BA-stimulated secretion of appetite and metabolism regulating hormones from the gut and pancreas is not well described and was the purpose of this study.

methodsThe effects of bile acids on the secretion of gut and pancreatic hormones was studied in rats and compared to the most well described nutritional secretagogue: glucose. The molecular mechanisms that underlie the secretion was studied by isolated perfused rat and mouse small intestine and pancreas preparations and supported by immunohistochemistry, expression analysis, and pharmacological studies.

resultsBile acids robustly stimulate secretion of not only the incretin hormones, glucose-dependent insulinotropic peptide (GIP), and glucagon-like peptide-1 (GLP-1), but also glucagon and insulin in vivo, to levels comparable to those resulting from glucose stimulation. The mechanisms of GLP-1, neurotensin, and peptide YY (PYY) secretion was secondary to intestinal absorption and depended on activation of basolateral membrane Takeda G-protein receptor 5 (TGR5) receptors on the L-cells in the following order of potency: Lithocholic acid (LCA) >Deoxycholicacid (DCA)>Chenodeoxycholicacid (CDCA)> Cholic acid (CA). Thus BAs did not stimulate secretion of GLP-1 and PYY from perfused small intestine in TGR5 KO mice but stimulated robust responses in wild type littermates. TGR5 is not expressed on α-cells or β-cells, and BAs had no direct effects on glucagon or insulin secretion from the perfused pancreas.

conclusionBAs should be considered not only as fat emulsifiers but also as important regulators of appetite- and metabolism-regulating hormones by activation of basolateral intestinal TGR5.

Indexed as

AnimalsBile Acids and SaltsCells, CulturedChlorocebus aethiopsCOS CellsGastric Inhibitory PolypeptideGlucagon-Like Peptide 1Intestinal MucosaMaleMiceMice, Inbred C57BLPancreasPeptide YYRatsRats, WistarReceptors, G-Protein-CoupledBile Acids and SaltsGastric Inhibitory PolypeptideGlucagon-Like Peptide 1Gpbar1 protein, mousePeptide YYReceptors, G-Protein-CoupledBile-acidsGLP-1InsulinNeurotensinPYYTGR5

Identifiers

PMID29656109
PMCPMC6001409
OpenAlexW2800295644

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.