Evidence map›Paper›PMID 25325736›Full record

ArticleDiabetes2015

Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1.

Edward C Emery, Eleftheria Diakogiannaki, Clive Gentry, Arianna Psichas, Abdella M Habib, Stuart Bevan, Michael J M Fischer, Frank Reimann, Fiona M Gribble

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 67 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Cellular mechanisms of incretin hormone secretion.Journal of molecular endocrinology · 2024
    Review
  7. Review
  8. Article
  9. Inflammation-the role of TRPA1 channel.Frontiers in physiology · 2023
    Review
  10. Article
  11. Review
  12. Article
  13. Boosting GLP-1 by Natural Products.Advances in experimental medicine and biology · 2021
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. TRPM6 N-Terminal CaM- and S100A1-Binding Domains.International journal of molecular sciences · 2019
    Article
  19. Review
  20. 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

9 authors at 1 institution in 1 country.

Edward C EmeryCambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge, U.K.
Eleftheria DiakogiannakiCambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge, U.K.
Clive GentryWolfson Centre for Age-Related Diseases, King's College London, London, U.K.
Arianna PsichasCambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge, U.K.
Abdella M HabibMolecular Nociception Group, Wolfson Institute for Biomedical Research, University College London, London, U.K.
Stuart BevanWolfson Centre for Age-Related Diseases, King's College London, London, U.K.
Michael J M FischerInstitute of Physiology and Pathophysiology, University of Erlangen-Nuremberg, Erlangen, Germany.
Frank ReimannCambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge, U.K. fmg23@cam.ac.uk fr222@cam.ac.uk.
Fiona M GribbleCambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge, U.K. fmg23@cam.ac.uk fr222@cam.ac.uk.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

Medical Research Council MC_UU_12012/3Medical Research Council MC_UU_12012/5Wellcome Trust 084210Wellcome Trust 088357Wellcome Trust WT084210/Z/07/ZWellcome Trust WT088357/Z/09/Z
6 · The paper itself

Abstract

Stimulus-coupled incretin secretion from enteroendocrine cells plays a fundamental role in glucose homeostasis and could be targeted for the treatment of type 2 diabetes. Here, we investigated the expression and function of transient receptor potential (TRP) ion channels in enteroendocrine L cells producing GLP-1. By microarray and quantitative PCR analysis, we identified trpa1 as an L cell-enriched transcript in the small intestine. Calcium imaging of primary L cells and the model cell line GLUTag revealed responses triggered by the TRPA1 agonists allyl-isothiocyanate (mustard oil), carvacrol, and polyunsaturated fatty acids, which were blocked by TRPA1 antagonists. Electrophysiology in GLUTag cells showed that carvacrol induced a current with characteristics typical of TRPA1 and triggered the firing of action potentials. TRPA1 activation caused an increase in GLP-1 secretion from primary murine intestinal cultures and GLUTag cells, an effect that was abolished in cultures from trpa1(-/-) mice or by pharmacological TRPA1 inhibition. These findings present TRPA1 as a novel sensory mechanism in enteroendocrine L cells, coupled to the facilitation of GLP-1 release, which may be exploitable as a target for treating diabetes.

Indexed as

AnimalsCalciumCells, CulturedEnteroendocrine CellsGlucagon-Like Peptide 1Intestine, SmallMiceMice, KnockoutSignal TransductionTransient Receptor Potential ChannelsTRPA1 Cation ChannelCalciumGlucagon-Like Peptide 1Transient Receptor Potential ChannelsTRPA1 Cation ChannelTrpa1 protein, mouse

Identifiers

PMID25325736
PMCPMC4375100
OpenAlexW2121876093

What OpenQuestion holds

Textmetadata
LicenceTDM
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.