Evidence map›Paper›PMID 30187652›Full record

ArticlePhysiological reports2018

GLP-1 suppresses glucagon secretion in human pancreatic alpha-cells by inhibition of P/Q-type Ca

Reshma Ramracheya, Caroline Chapman, Margarita Chibalina, Haiqiang Dou, Caroline Miranda, Alejandro González, Yusuke Moritoh, Makoto Shigeto, Quan Zhang, Matthias Braun and 4 more

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Glucagon-Like Peptide-1 Receptor Agonists in Type 2 Diabetes Mellitus and Cardiovascular Disease: The Past, Present, and Future.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2022
    Pooled it
  2. Postnatal refinement of CaChannels (Austin, Tex.) · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

6 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

14 authors at 4 institutions in 2 countries.

Reshma RamracheyaOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Caroline ChapmanOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Margarita ChibalinaOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Haiqiang DouInstitute of Neuroscience and Physiology, Metabolic Research Unit, University of Göteborg, Göteborg, Sweden.
Caroline MirandaInstitute of Neuroscience and Physiology, Metabolic Research Unit, University of Göteborg, Göteborg, Sweden.
Alejandro GonzálezOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Yusuke MoritohOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Makoto ShigetoOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Quan ZhangOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Matthias BraunOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Anne ClarkOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Paul R JohnsonNuffield Department of Surgery, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom.
Patrik RorsmanOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Linford J B BriantOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
University of Oxford · GBOxford Centre for Diabetes, Endocrinology and Metabolism · GBUniversity of Gothenburg · SEOxford BioMedica (United Kingdom) · GB

Funding

Diabetes UKMedical Research Council G0801995Wellcome Trust 089795Wellcome Trust 095531Wellcome Trust 095531/Z/11/ZWellcome Trust 201325/Z/16/ZWellcome Trust 884655
6 · The paper itself

Abstract

Glucagon is the body's main hyperglycemic hormone, and its secretion is dysregulated in type 2 diabetes mellitus (T2DM). The incretin hormone glucagon-like peptide-1 (GLP-1) is released from the gut and is used in T2DM therapy. Uniquely, it both stimulates insulin and inhibits glucagon secretion and thereby lowers plasma glucose levels. In this study, we have investigated the action of GLP-1 on glucagon release from human pancreatic islets. Immunocytochemistry revealed that only <0.5% of the α-cells possess detectable GLP-1R immunoreactivity. Despite this, GLP-1 inhibited glucagon secretion by 50-70%. This was due to a direct effect on α-cells, rather than paracrine signaling, because the inhibition was not reversed by the insulin receptor antagonist S961 or the somatostatin receptor-2 antagonist CYN154806. The inhibitory effect of GLP-1 on glucagon secretion was prevented by the PKA-inhibitor Rp-cAMPS and mimicked by the adenylate cyclase activator forskolin. Electrophysiological measurements revealed that GLP-1 decreased action potential height and depolarized interspike membrane potential. Mathematical modeling suggests both effects could result from inhibition of P/Q-type Ca

Indexed as

AdultAnimalsCalcium Channel BlockersCalcium Channels, P-TypeCalcium Channels, Q-TypeCells, CulturedExocytosisFemaleGlucagonGlucagon-Like Peptide 1Glucagon-Secreting CellsHumansMaleMembrane PotentialsMiceMiddle AgedCalcium Channel BlockersCalcium Channels, P-TypeCalcium Channels, Q-TypeGlucagonGlucagon-Like Peptide 1cAMP, cyclic adenosine monophosphateGLP-1, glucagon-like peptide 1KATP, potassium ATP channelSST, somatostatinT2DM, Type 2 diabetes mellitus

Identifiers

PMID30187652
PMCPMC6125244
OpenAlexW2892229332

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.