Evidence map›Paper›PMID 21716694›Full record

ReviewExperimental diabetes research2011

Activation of the GLP-1 receptor signalling pathway: a relevant strategy to repair a deficient beta-cell mass.

Bernard Portha, Cécile Tourrel-Cuzin, Jamileh Movassat

Abstract readReview
In one paragraph

Review in Experimental diabetes research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
–field-weighted citation impact
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

38 citing papers in PubMed.

  1. Trial
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  11. Article
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  13. Glucagon-like peptide-1 receptor: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024 · on this map
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Signaling pathways in obesity: mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022
    Review
  19. Article
  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

3 authors.

Bernard PorthaLaboratoire B2PE (Biologie et Pathologie du Pancréas Endocrine), Unité BFA (Biologie Fonctionnelle et Adaptive), Equipe 1, Université Paris-Diderot et CNRS EAC 4413, Bâtiment BUFFON, 5ème étage, pièce 552A, 4, Rue Lagroua Weill Hallé, Case 7126, 75205 Paris Cedex 13, France.
Cécile Tourrel-Cuzin
Jamileh Movassat

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent preclinical studies in rodent models of diabetes suggest that exogenous GLP-1R agonists and DPP-4 inhibitors have the ability to increase islet mass and preserve beta-cell function, by immediate reactivation of beta-cell glucose competence, as well as enhanced beta-cell proliferation and neogenesis and promotion of beta-cell survival. These effects have tremendous implication in the treatment of T2D because they directly address one of the basic defects in T2D, that is, beta-cell failure. In human diabetes, however, evidence that the GLP-1-based drugs alter the course of beta-cell function remains to be found. Several questions surrounding the risks and benefits of GLP-1-based therapy for the diabetic beta-cell mass are discussed in this review and require further investigation.

Indexed as

AnimalsCell Transformation, NeoplasticDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2FemaleGlucagon-Like Peptide-1 ReceptorHumansInsulin-Secreting CellsMiddle AgedPancreatic NeoplasmsPancreatitisRatsReceptors, GlucagonSignal TransductionGLP1R protein, humanGlp1r protein, ratGlucagon-Like Peptide-1 ReceptorReceptors, Glucagon

Identifiers

PMID21716694
PMCPMC3118608

What OpenQuestion holds

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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 OpenQuestion graph.