Evidence map›Paper›PMID 27044660›Full record

ReviewUpsala journal of medical sciences2016

Glucose control of glucagon secretion-'There's a brand-new gimmick every year'.

Erik Gylfe

Open access · diamondAbstract readReview
In one paragraph

Review in Upsala journal of medical sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
9.4field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Pancreatic δ Cells: An Overlooked Cell in Focus.Advances in anatomy, embryology, and cell biology · 2024
    Review
  7. Article
  8. Metabolic regulation of glucagon secretion.The Journal of endocrinology · 2023
    Article
  9. Review
  10. Review
  11. Article
  12. Metabolic Messengers: glucagon.Nature metabolism · 2023
    Review
  13. Article
  14. Liraglutide increases islet CaDiabetes, obesity & metabolism · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  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

1 author at 1 institution in 1 country.

Erik Gylfea Department of Medical Cell Biology , Uppsala University , Uppsala , Sweden.
Uppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucagon from the pancreatic α-cells is a major blood glucose-regulating hormone whose most important role is to prevent hypoglycaemia that can be life-threatening due to the brain's strong dependence on glucose as energy source. Lack of blood glucose-lowering insulin after malfunction or autoimmune destruction of the pancreatic β-cells is the recognized cause of diabetes, but recent evidence indicates that diabetic hyperglycaemia would not develop unless lack of insulin was accompanied by hypersecretion of glucagon. Glucagon release has therefore become an increasingly important target in diabetes management. Despite decades of research, an understanding of how glucagon secretion is regulated remains elusive, and fundamentally different mechanisms continue to be proposed. The autonomous nervous system is an important determinant of glucagon release, but it is clear that secretion is also directly regulated within the pancreatic islets. The present review focuses on pancreatic islet mechanisms involved in glucose regulation of glucagon release. It will be argued that α-cell-intrinsic processes are most important for regulation of glucagon release during recovery from hypoglycaemia and that paracrine inhibition by somatostatin from the δ-cells shapes pulsatile glucagon release in hyperglycaemia. The electrically coupled β-cells ultimately determine islet hormone pulsatility by releasing synchronizing factors that affect the α- and δ-cells.

Indexed as

AnimalsAutoimmune DiseasesBlood GlucoseDiabetes Mellitus, ExperimentalDose-Response Relationship, DrugGlucagonGlucagon-Secreting CellsGlucoseHumansHyperglycemiaInsulinInsulin-Secreting CellsIslets of LangerhansMiceSignal TransductionSomatostatinBlood GlucoseGlucagonGlucoseInsulinSomatostatinDiabetesglucagon secretionglucose homeostasissignal transduction

Identifiers

PMID27044660
PMCPMC4900067
OpenAlexW2335870747

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.