Evidence map›Paper›PMID 32477262›Full record

ArticleFrontiers in endocrinology2020

Repurposed Analog of GLP-1 Ameliorates Hyperglycemia in Type 1 Diabetic Mice Through Pancreatic Cell Reprogramming.

Adrian Villalba, Silvia Rodriguez-Fernandez, David Perna-Barrull, Rosa-Maria Ampudia, Laia Gomez-Muñoz, Irma Pujol-Autonell, Eva Aguilera, Mireia Coma, Mary Cano-Sarabia, Federico Vázquez and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. 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

12 authors at 5 institutions in 1 country.

Adrian VillalbaImmunology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Silvia Rodriguez-FernandezImmunology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
David Perna-BarrullImmunology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Rosa-Maria AmpudiaImmunology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Laia Gomez-MuñozImmunology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Irma Pujol-AutonellImmunology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Eva AguileraEndocrinology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Mireia ComaAnaxomics Biotech SL, Barcelona, Spain.
Mary Cano-SarabiaCatalan Institute of Nanoscience and Nanotechnology, CSIC and The Barcelona Institute of Science and Technology, Bellaterra, Spain.
Federico VázquezEndocrinology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Joan VerdaguerImmunology Unit, Department of Experimental Medicine, Faculty of Medicine, IRBLleida, University of Lleida, Lleida, Spain.
Marta Vives-PiImmunology Section, Germans Trias i Pujol Research Institute, Autonomous University of Barcelona, Badalona, Spain.
Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol · ESUniversitat Autònoma de Barcelona · ESAnaxomics (Spain) · ESInstitut Català de Nanociència i Nanotecnologia · ESInstituto de Investigación Biomédica de Lleida · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes is an autoimmune disease caused by the destruction of the insulin-producing β-cells. An ideal immunotherapy should combine the blockade of the autoimmune response with the recovery of functional target cell mass. With the aim to develop new therapies for type 1 diabetes that could contribute to β-cell mass restoration, a drug repositioning analysis based on systems biology was performed to identify the β-cell regenerative potential of commercially available compounds. Drug repositioning is a strategy used for identifying new uses for approved drugs that are outside the scope of the medical indication. A list of 28 non-synonymous repurposed drug candidates was obtained, and 16 were selected as diabetes mellitus type 1 treatment candidates regarding pancreatic β-cell regeneration. Drugs with poor safety profile were further filtered out. Lastly, we selected liraglutide for its predictive efficacy values for neogenesis, transdifferentiation of α-cells, and/or replication of pre-existing β-cells. Liraglutide is an analog of glucagon-like peptide-1, a drug used in patients with type 2 diabetes. Liraglutide was tested in immunodeficient NOD-

Indexed as

Cellular ReprogrammingAnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Glucagon-Like Peptide 1HyperglycemiaHypoglycemic AgentsInsulin-Secreting CellsLiraglutideMaleMiceMice, Inbred NODMice, SCIDGlucagon-Like Peptide 1Hypoglycemic AgentsLiraglutidebeta cell regenerationdrug repositioningliraglutideneogenesistransdifferentiation

Identifiers

PMID32477262
PMCPMC7237704
OpenAlexW3024937199

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.