Evidence map›Paper›PMID 30310153›Full record

ReviewNature reviews. Endocrinology2018

The α-cell in diabetes mellitus.

Jesper Gromada, Pauline Chabosseau, Guy A Rutter

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
12.3field-weighted citation impact, top 1% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. mNature metabolism · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Hypothalamus-liver talks: whispers in the language of metabolism.Reviews in endocrine & metabolic disorders · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. [Advances in injectable and transdermal glucose-responsive insulin delivery systems].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Insulin resistance in type 2 diabetes mellitus.Nature reviews. Endocrinology · 2025
    Review
  19. Article
  20. Article

24 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

3 authors at 2 institutions in 2 countries.

Jesper GromadaRegeneron Pharmaceuticals, Tarrytown, NY, USA. jesper.gromada@regeneron.com.
Pauline ChabosseauSection of Cell Biology and Functional Genomics, Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Imperial College London, Hammersmith Hospital Campus, London, UK.
Guy A RutterSection of Cell Biology and Functional Genomics, Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Imperial College London, Hammersmith Hospital Campus, London, UK. g.rutter@imperial.ac.uk.ORCID http://orcid.org/0000-0001-6360-0343
Hammersmith Hospital · GBRegeneron (United States) · US

Funding

Medical Research Council MR/K001981/1Medical Research Council MR/K023667/1Medical Research Council MR/L020149/1Medical Research Council MR/L02036X/1Medical Research Council MR/M012646/1Medical Research Council MR/N00275X/1Medical Research Council MR/N020472/1Medical Research Council MR/R010676/1
6 · The paper itself

Abstract

Findings from the past 10 years have placed the glucagon-secreting pancreatic α-cell centre stage in the development of diabetes mellitus, a disease affecting almost one in every ten adults worldwide. Glucagon secretion is reduced in patients with type 1 diabetes mellitus, increasing the risk of insulin-induced hypoglycaemia, but is enhanced in type 2 diabetes mellitus, exacerbating the effects of diminished insulin release and action on blood levels of glucose. A better understanding of the mechanisms underlying these changes is therefore an important goal. RNA sequencing reveals that, despite their opposing roles in the control of blood levels of glucose, α-cells and β-cells have remarkably similar patterns of gene expression. This similarity might explain the fairly facile interconversion between these cells and the ability of the α-cell compartment to serve as a source of new β-cells in models of extreme β-cell loss that mimic type 1 diabetes mellitus. Emerging data suggest that GABA might facilitate this interconversion, whereas the amino acid glutamine serves as a liver-derived factor to promote α-cell replication and maintenance of α-cell mass. Here, we survey these developments and their therapeutic implications for patients with diabetes mellitus.

Indexed as

Diabetes Mellitus, Type 1Diabetes Mellitus, Type 2FemaleGlucagonGlucagon-Secreting CellsHumansInsulinInsulin-Secreting CellsMaleRoleSensitivity and SpecificityGlucagonInsulin

Identifiers

PMID30310153
OpenAlexW2897922438

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.