Evidence map›Paper›PMID 26565000›Full record

ArticleGut2017

Apelin targets gut contraction to control glucose metabolism via the brain.

Audren Fournel, Anne Drougard, Thibaut Duparc, Alysson Marlin, Stuart M Brierley, Joel Castro, Sophie Le-Gonidec, Bernard Masri, André Colom, Alexandre Lucas and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Gut, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Article
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  8. Review
  9. Review
  10. Nutrients · 2023
    Article
  11. Review
  12. PasteurizedHeliyon · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Role of the gut-brain axis in energy and glucose metabolism.Experimental & molecular medicine · 2022
    Review
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

16 authors at 8 institutions in 4 countries.

Audren FournelInstitut National de la Santé et de la Recherche Médicale (INSERM), U1048, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Toulouse Cedex 4, France.
Anne DrougardInstitut National de la Santé et de la Recherche Médicale (INSERM), U1048, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Toulouse Cedex 4, France.
Thibaut DuparcNeuroMicrobiota, European Associated Laboratory (EAL) INSERM/UCL.
Alysson MarlinInstitut National de la Santé et de la Recherche Médicale (INSERM), U1048, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Toulouse Cedex 4, France.
Stuart M BrierleyVisceral Pain Group, Centre for Nutrition and Gastrointestinal Diseases, Discipline of Medicine, University of Adelaide, South Australia Health and Medical Research Institute (SAHMRI), Adelaide, South Australia, Australia.
Joel CastroVisceral Pain Group, Centre for Nutrition and Gastrointestinal Diseases, Discipline of Medicine, University of Adelaide, South Australia Health and Medical Research Institute (SAHMRI), Adelaide, South Australia, Australia.
Sophie Le-GonidecInstitut National de la Santé et de la Recherche Médicale (INSERM), U1048, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Toulouse Cedex 4, France.
Bernard MasriInstitut National de la Santé et de la Recherche Médicale (INSERM), U1037, Centre de Recherches en Cancérologie de Toulouse (CRCT), CHU Rangueil, Toulouse, Cedex 4, France.
André ColomInstitut National de la Santé et de la Recherche Médicale (INSERM), U1048, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Toulouse Cedex 4, France.
Alexandre LucasInstitut National de la Santé et de la Recherche Médicale (INSERM), U1048, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Toulouse Cedex 4, France.
Perrine RoussetUniversité Paul Sabatier, Toulouse, France.
Nicolas CenacUniversité Paul Sabatier, Toulouse, France.
Nathalie VergnolleUniversité Paul Sabatier, Toulouse, France.
Philippe ValetInstitut National de la Santé et de la Recherche Médicale (INSERM), U1048, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Toulouse Cedex 4, France.
Patrice D CaniNeuroMicrobiota, European Associated Laboratory (EAL) INSERM/UCL.
Claude KnaufInstitut National de la Santé et de la Recherche Médicale (INSERM), U1048, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Toulouse Cedex 4, France.
Associated Research (United States) · USInserm · FRUniversité Toulouse III - Paul Sabatier · FRCentre de Physiopathologie de Toulouse-Purpan · FRCentre de Recherche en Cancérologie de Toulouse · FRInstitut des Maladies Métaboliques et Cardiovasculaires · FRSouth Australian Health and Medical Research Institute · AUThe University of Adelaide · AU

Funding

European Research Council 336452
6 · The paper itself

Abstract

objectiveThe gut-brain axis is considered as a major regulatory checkpoint in the control of glucose homeostasis. The detection of nutrients and/or hormones in the duodenum informs the hypothalamus of the host's nutritional state. This process may occur via hypothalamic neurons modulating central release of nitric oxide (NO), which in turn controls glucose entry into tissues. The enteric nervous system (ENS) modulates intestinal contractions in response to various stimuli, but the importance of this interaction in the control of glucose homeostasis via the brain is unknown. We studied whether apelin, a bioactive peptide present in the gut, regulates ENS-evoked contractions, thereby identifying a new physiological partner in the control of glucose utilisation via the hypothalamus.

designWe measured the effect of apelin on electrical and mechanical duodenal responses via telemetry probes and isotonic sensors in normal and obese/diabetic mice. Changes in hypothalamic NO release, in response to duodenal contraction modulated by apelin, were evaluated in real time with specific amperometric probes. Glucose utilisation in tissues was measured with orally administrated radiolabeled glucose.

resultsIn normal and obese/diabetic mice, glucose utilisation is improved by the decrease of ENS/contraction activities in response to apelin, which generates an increase in hypothalamic NO release. As a consequence, glucose entry is significantly increased in the muscle.

conclusionsHere, we identify a novel mode of communication between the intestine and the hypothalamus that controls glucose utilisation. Moreover, our data identified oral apelin administration as a novel potential target to treat metabolic disorders.

Indexed as

AdipokinesAnimalsApelinBiosensing TechniquesDiabetes MellitusDuodenumEnteric Nervous SystemGastrointestinal MotilityGlucoseHomeostasisHypothalamusIntercellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLMuscle ContractionAdipokinesApelinApln protein, mouseGlucoseIntercellular Signaling Peptides and ProteinsNitric OxideENTERIC NERVOUS SYSTEMGASTROINTESTINAL PHYSIOLOGYGLUCOSE METABOLISMGUT HORMONESOBESITY

Identifiers

PMID26565000
PMCPMC5284480
OpenAlexW2201278029

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.