Evidence map›Paper›PMID 24766140›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2014

Incretin-modulated beta cell energetics in intact islets of Langerhans.

David J Hodson, Andrei I Tarasov, Silvia Gimeno Brias, Ryan K Mitchell, Natalie R Johnston, Shahab Haghollahi, Matthew C Cane, Marco Bugliani, Piero Marchetti, Domenico Bosco and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
9.1field-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

41 citing papers in PubMed, 67 citations in OpenAlex.

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  13. PDX1Nature communications · 2021
    Article
  14. The Pancreatic β-Cell: The Perfect Redox System.Antioxidants (Basel, Switzerland) · 2021
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Mechanisms of the Regulation and Dysregulation of Glucagon Secretion.Oxidative medicine and cellular longevity · 2020
    Review
  20. Review
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

13 authors at 5 institutions in 3 countries.

David J HodsonSection of Cell Biology, Division of Diabetes, Endocrinology and Metabolism, Department of Medicine (D.J.H, A.I.T., S.G.B., R.K.M., N.R.J., S.H., M.C.C., G.A.R.), Imperial College London, London W12 0NN, United Kingdom; Department of Endocrinology and Metabolism (M.B., P.M.), University of Pisa, 56126 Pisa, Italy; Cell Isolation and Transplantation Center, Department of Surgery (D.B.), Geneva University Hospitals and University of Geneva, 1205 Geneva, Switzerland; Oxford Centre for Diabetes, Endocrinology, & Metabolism (P.R.J., S.J.H.), University of Oxford, Oxford OX3 7LE, United Kingdom; NIHR Oxford Biomedical Research Centre (P.R.J., S.J.H.), Churchill Hospital, Oxford OX3 7LE, United Kingdom; and Nuffield Department of Surgical Sciences (P.R.J., S.J.H.), University of Oxford, Oxford OX3 9DU, United Kingdom.
Andrei I Tarasov
Silvia Gimeno Brias
Ryan K Mitchell
Natalie R Johnston
Shahab Haghollahi
Matthew C Cane
Marco Bugliani
Piero Marchetti
Domenico Bosco
Paul R Johnson
Stephen J Hughes
Guy A Rutter
Imperial College London · GBUniversity of Pisa · ITOxford Centre for Diabetes, Endocrinology and Metabolism · GBUniversity Hospital of Geneva · CHUniversity of Oxford · GB

Funding

Biotechnology and Biological Sciences Research Council BB/J015873/1Medical Research Council MR/J0003042/1Wellcome Trust 098424Wellcome Trust WT098424AIA
6 · The paper itself

Abstract

Incretins such as glucagon-like peptide 1 (GLP-1) are released from the gut and potentiate insulin release in a glucose-dependent manner. Although this action is generally believed to hinge on cAMP and protein kinase A signaling, up-regulated beta cell intermediary metabolism may also play a role in incretin-stimulated insulin secretion. By employing recombinant probes to image ATP dynamically in situ within intact mouse and human islets, we sought to clarify the role of GLP-1-modulated energetics in beta cell function. Using these techniques, we show that GLP-1 engages a metabolically coupled subnetwork of beta cells to increase cytosolic ATP levels, an action independent of prevailing energy status. We further demonstrate that the effects of GLP-1 are accompanied by alterations in the mitochondrial inner membrane potential and, at elevated glucose concentration, depend upon GLP-1 receptor-directed calcium influx through voltage-dependent calcium channels. Lastly, and highlighting critical species differences, beta cells within mouse but not human islets respond coordinately to incretin stimulation. Together, these findings suggest that GLP-1 alters beta cell intermediary metabolism to influence ATP dynamics in a species-specific manner, and this may contribute to divergent regulation of the incretin-axis in rodents and man.

Indexed as

Adenosine TriphosphateAdultAnimalsCalcium SignalingEnergy MetabolismGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucoseHumansIncretinsInsulin-Secreting CellsMembrane Potential, MitochondrialMiceMiddle AgedReceptors, GlucagonSpecies SpecificityAdenosine TriphosphateGLP1R protein, humanGlp1r protein, mouseGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucoseIncretinsReceptors, Glucagon

Identifiers

PMID24766140
PMCPMC4042069
OpenAlexW2153956170

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.