Evidence map›Paper›PMID 32269764›Full record

ReviewF1000Research2020

Recent advances in understanding the role of glucagon-like peptide 1.

Josh Reed, Stephen Bain, Venkateswarlu Kanamarlapudi

Open access · goldAbstract readReview
In one paragraph

Review in F1000Research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  4. Article
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  6. Observational
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  8. Review
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  10. Review
  11. Article
  12. GLP-1 in the Hypothalamic Paraventricular Nucleus Promotes Sympathetic Activation and Hypertension.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Neuroprotective effects of an engineeredBioengineering & translational medicine · 2023
    Article
  18. 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 at 1 institution in 1 country.

Josh ReedInstitute of Life Science, Medical School, Swansea University, Swansea, Wales, SA2 8PP, UK.
Stephen BainInstitute of Life Science, Medical School, Swansea University, Swansea, Wales, SA2 8PP, UK.
Venkateswarlu KanamarlapudiInstitute of Life Science, Medical School, Swansea University, Swansea, Wales, SA2 8PP, UK.ORCID 0000-0002-8739-1483
Swansea University · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F017596/1
6 · The paper itself

Abstract

The discovery that glucagon-like peptide 1 (GLP-1) mediates a significant proportion of the incretin effect during the postprandial period and the subsequent observation that GLP-1 bioactivity is retained in type 2 diabetes (T2D) led to new therapeutic strategies being developed for T2D treatment based on GLP-1 action. Although owing to its short half-life exogenous GLP-1 has no use therapeutically, GLP-1 mimetics, which have a much longer half-life than native GLP-1, have proven to be effective for T2D treatment since they prolong the incretin effect in patients. These GLP-1 mimetics are a desirable therapeutic option for T2D since they do not provoke hypoglycaemia or weight gain and have simple modes of administration and monitoring. Additionally, over more recent years, GLP-1 action has been found to mediate systemic physiological beneficial effects and this has high clinical relevance due to the post-diagnosis complications of T2D. Indeed, recent studies have found that certain GLP-1 analogue therapies improve the cardiovascular outcomes for people with diabetes. Furthermore, GLP-1-based therapies may enable new therapeutic strategies for diseases that can also arise independently of the clinical manifestation of T2D, such as dementia and Parkinson's disease. GLP-1 functions by binding to its receptor (GLP-1R), which expresses mainly in pancreatic islet beta cells. A better understanding of the mechanisms and signalling pathways by which acute and chronic GLP-1R activation alleviates disease phenotypes and induces desirable physiological responses during healthy conditions will likely lead to the development of new therapeutic GLP-1 mimetic-based therapies, which improve prognosis to a greater extent than current therapies for an array of diseases.

Indexed as

Diabetes Mellitus, Type 2Insulin-Secreting CellsGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorHumansHypoglycemic AgentsIncretinsGLP1R protein, humanGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorHypoglycemic AgentsIncretinsGLP-1GLP-1RincretinType 2 diabetes

Identifiers

PMID32269764
PMCPMC7137394
OpenAlexW3014700813

What OpenQuestion holds

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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.