Evidence map›Paper›PMID 26696515›Full record

ReviewBest practice & research. Clinical endocrinology & metabolism2015

Evolving function and potential of pancreatic alpha cells.

Violeta Stanojevic, Joel F Habener

Abstract readReview
In one paragraph

Review in Best practice & research. Clinical endocrinology & metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.5field-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

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Beneficial Effects of ProbioticInternational journal of molecular sciences · 2024
    Article
  9. Zinc-chelating BET bromodomain inhibitors equally target islet endocrine cell types.American journal of physiology. Regulatory, integrative and comparative physiology · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Regulation of α-cell glucagon secretion: The role of second messengers.Chronic diseases and translational medicine · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Alpha the versatile: Guardians of the islets.Journal of diabetes investigation · 2019
    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

2 authors at 1 institution in 1 country.

Violeta StanojevicLaboratory of Molecular Endocrinology, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Joel F HabenerLaboratory of Molecular Endocrinology, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Electronic address: jhabener@mgh.harvard.edu.
Harvard University · US

Funding

Transgenic CoreP30DK057521 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI FLOREZ, JOSE CARLOS · 2000 to 2019
$31.4M
NIDDK NIH HHS P30 DK057521
6 · The paper itself

Abstract

The alpha cells that co-occupy the islets in association with beta cells have been long recognized as the source of glucagon, a hyperglycemia-producing and diabetogenic hormone. Although the mechanisms that control the functions of alpha cells, glucagon secretion, and the role of glucagon in diabetes have remained somewhat enigmatic over the fifty years since their discovery, seminal findings during the past few years have moved alpha cells into the spotlight of scientific discovery. These findings obtained largely from studies in mice are: Alpha cells have the capacity to trans-differentiate into insulin-producing beta cells. Alpha cells contain a GLP-1 generating system that produces GLP-1 locally for paracrine actions within the islets that likely promotes beta cell growth and survival and maintains beta cell mass. Impairment of glucagon signaling both prevents the occurrence of diabetes in conditions of the near absence of insulin and expands alpha cell mass. Alpha cells appear to serve as helper cells or guardians of beta cells to ensure their health and well-being. Of potential relevance to the possibility of promoting the transformation of alpha to beta cells is the observation that impairment of glucagon signaling leads to a marked increase in alpha cell mass in the islets. Such alpha cell hyperplasia provides an increased supply of alpha cells for their transdifferentiation into new beta cells. In this review we discuss these recent discoveries from the perspective of their potential relevance to the treatment of diabetes.

Indexed as

Cell TransdifferentiationAnimalsGlucagonGlucagon-Secreting CellsHumansInsulin-Secreting CellsSignal TransductionGlucagonalpha cellsbeta cellsdiabetesGLP-1proglucagontransdifferentiation

Identifiers

PMID26696515
PMCPMC4690008
OpenAlexW2200420822

What OpenQuestion holds

Textmetadata
LicenceTDM
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.