Evidence map›Paper›PMID 22262074›Full record

ReviewThe review of diabetic studies : RDS2011

The alpha-cell as target for type 2 diabetes therapy.

Mikkel Christensen, Jonatan I Bagger, Tina Vilsbøll, Filip K Knop

Open access · bronzeAbstract readReview
In one paragraph

Review in The review of diabetic studies : RDS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
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  6. Incretin and glucagon receptor polypharmacology in chronic kidney disease.American journal of physiology. Endocrinology and metabolism · 2024
    Review
  7. Review
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  9. Review
  10. Review
  11. Article
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  16. Regulation of islet glucagon secretion: Beyond calcium.Diabetes, obesity & metabolism · 2018
    Review
  17. Article
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  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

4 authors at 2 institutions in 1 country.

Mikkel ChristensenDiabetes Research Division, Department of Internal Medicine F, Gentofte Hospital, University of Copenhagen, Denmark.
Jonatan I Bagger
Tina Vilsbøll
Filip K Knop
Gentofte Hospital · DKUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucagon is the main secretory product of the pancreatic alpha-cells. The main function of this peptide hormone is to provide sustained glucose supply to the brain and other vital organs during fasting conditions. This is exerted by stimulation of hepatic glucose production via specific G protein-coupled receptors in the hepatocytes. Type 2 diabetic patients are characterized by elevated glucagon levels contributing decisively to hyperglycemia in these patients. Accumulating evidence demonstrates that targeting the pancreatic alpha-cell and its main secretory product glucagon is a possible treatment for type 2 diabetes. Several lines of preclinical evidence have paved the way for the development of drugs, which suppress glucagon secretion or antagonize the glucagon receptor. In this review, the physiological actions of glucagon and the role of glucagon in type 2 diabetic pathophysiology are outlined. Furthermore, potential advantages and limitations of antagonizing the glucagon receptor or suppressing glucagon secretion in the treatment of type 2 diabetes are discussed with a focus on already marketed drugs and drugs in clinical development. It is concluded that the development of novel glucagon receptor antagonists are confronted with several safety issues. At present, available pharmacological agents based on the glucose-dependent glucagonostatic effects of GLP-1 represent the most favorable way to apply constraints to the alpha-cell in type 2 diabetes.

Indexed as

AnimalsDiabetes Mellitus, Type 2GlucagonGlucagon-Secreting CellsHumansHypoglycemic AgentsReceptors, GlucagonGlucagonHypoglycemic AgentsReceptors, Glucagon

Identifiers

PMID22262074
PMCPMC3280671
OpenAlexW1572696163

What OpenQuestion 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 OpenQuestion graph.