Evidence mapPaperPMID 36932176Full record

ReviewNature reviews. Endocrinology2023

Revisiting the role of glucagon in health, diabetes mellitus and other metabolic diseases.

Sofie Hædersdal, Andreas Andersen, Filip K Knop, Tina Vilsbøll

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing 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

62 citing papers in PubMed.

  1. Trial
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  5. Article
  6. Effects of Glucagon-Like Peptide-1 Receptor Agonists (Mono and Combination Therapy) on Energy Expenditure: A Scoping Review.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Impact of obesity on aromatic amino acids and brain glucose during acute hyperglycemia.American journal of physiology. Endocrinology and metabolism · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

2 more citing papers are in PubMed but not listed here.

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

4 authors.

Sofie HædersdalClinical Research, Copenhagen University Hospital - Steno Diabetes Center Copenhagen, Herlev, Denmark. sofie.haedersdal@regionh.dk.
Andreas AndersenClinical Research, Copenhagen University Hospital - Steno Diabetes Center Copenhagen, Herlev, Denmark.ORCID http://orcid.org/0000-0001-8190-5140
Filip K KnopClinical Research, Copenhagen University Hospital - Steno Diabetes Center Copenhagen, Herlev, Denmark.ORCID http://orcid.org/0000-0002-2495-5034
Tina VilsbøllClinical Research, Copenhagen University Hospital - Steno Diabetes Center Copenhagen, Herlev, Denmark. tina.vilsboell.01@regionh.dk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin and glucagon exert opposing effects on glucose metabolism and, consequently, pancreatic islet β-cells and α-cells are considered functional antagonists. The intra-islet hypothesis has previously dominated the understanding of glucagon secretion, stating that insulin acts to inhibit the release of glucagon. By contrast, glucagon is a potent stimulator of insulin secretion and has been used to test β-cell function. Over the past decade, α-cells have received increasing attention due to their ability to stimulate insulin secretion from neighbouring β-cells, and α-cell-β-cell crosstalk has proven central for glucose homeostasis in vivo. Glucagon is not only the counter-regulatory hormone to insulin in glucose metabolism but also glucagon secretion is more susceptible to changes in the plasma concentration of certain amino acids than to changes in plasma concentrations of glucose. Thus, the actions of glucagon also include a central role in amino acid turnover and hepatic fat oxidation. This Review provides insights into glucagon secretion, with a focus on the local paracrine actions on glucagon and the importance of α-cell-β-cell crosstalk. We focus on dysregulated glucagon secretion in obesity, non-alcoholic fatty liver disease and type 2 diabetes mellitus. Lastly, the future potential of targeting hyperglucagonaemia and applying dual and triple receptor agonists with glucagon receptor-activating properties in combination with incretin hormone receptor agonism is discussed.

Indexed as

Diabetes Mellitus, Type 2GlucagonMetabolic DiseasesGlucagon-Secreting CellsGlucoseHumansInsulinGlucagonGlucoseInsulin

Identifiers

PMID36932176

What Socratic holds

Textmetadata
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 Socratic graph.