Evidence map›Paper›PMID 29898400›Full record

ArticleCell reports2018

CPT1a-Dependent Long-Chain Fatty Acid Oxidation Contributes to Maintaining Glucagon Secretion from Pancreatic Islets.

Linford J B Briant, Michael S Dodd, Margarita V Chibalina, Nils J G Rorsman, Paul R V Johnson, Peter Carmeliet, Patrik Rorsman, Jakob G Knudsen

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
11.1field-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

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Signaling architecture of the glucagon-like peptide-1 receptor.The Journal of clinical investigation · 2026
    Review
  6. Glycolytic activation of β-cell NaMolecular metabolism · 2026
    Article
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  19. Article
  20. Metabolic regulation of glucagon secretion.The Journal of endocrinology · 2023
    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

8 authors at 5 institutions in 3 countries.

Linford J B BriantOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 7LE, UK; Department of Computer Science, University of Oxford, Oxford OX1 3QD, UK.
Michael S DoddDepartment of Physiology, Anatomy & Genetics, University of Oxford, Parks Road, Oxford OX1 3PT, UK; Faculty of Health and Life Sciences, Coventry University, Coventry CV1 5FB, UK.
Margarita V ChibalinaOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 7LE, UK.
Nils J G RorsmanOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 7LE, UK.
Paul R V JohnsonOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 7LE, UK; Oxford National Institute for Health Research, Biomedical Research Centre, Churchill Hospital, Oxford OX3 7LJ, UK.
Peter CarmelietLaboratory of Angiogenesis and Vascular Metabolism, VIB-KU Leuven Center for Cancer Biology, Leuven, Belgium.
Patrik RorsmanOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 7LE, UK; Metabolic Research, Department of Neuroscience and Physiology, Sahlgrenska Academy, University of Göteborg, Box 433, 405 30 Göteborg, Sweden.
Jakob G KnudsenOxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 7LE, UK. Electronic address: jakob.knudsen@ocdem.ox.ac.uk.
University of Oxford · GBOxford Centre for Diabetes, Endocrinology and Metabolism · GBChurchill Hospital · GBCoventry University · GBVIB-KU Leuven Center for Cancer Biology · BE

Funding

European Research Council 322620Wellcome Trust 089795Wellcome Trust 095531/Z/11/ZWellcome Trust 201325/Z/16/Z
6 · The paper itself

Abstract

Glucagon, the principal hyperglycemic hormone, is secreted from pancreatic islet α cells as part of the counter-regulatory response to hypoglycemia. Hence, secretory output from α cells is under high demand in conditions of low glucose supply. Many tissues oxidize fat as an alternate energy substrate. Here, we show that glucagon secretion in low glucose conditions is maintained by fatty acid metabolism in both mouse and human islets, and that inhibiting this metabolic pathway profoundly decreases glucagon output by depolarizing α cell membrane potential and decreasing action potential amplitude. We demonstrate, by using experimental and computational approaches, that this is not mediated by the K

Indexed as

Adenosine TriphosphateAnimalsBlood GlucoseCarnitine O-PalmitoyltransferaseFatty AcidsGlucagonGlucoseHumansIslets of LangerhansKATP ChannelsMembrane PotentialsMetabolic Networks and PathwaysMiceMice, Inbred C57BLMice, KnockoutProtein IsoformsAdenosine TriphosphateBlood GlucoseCarnitine O-PalmitoyltransferaseCPT1B protein, mouseFatty AcidsGlucagonGlucoseKATP ChannelsProtein IsoformsRNA, Small InterferingSodium-Potassium-Exchanging ATPaseCa2+fastingglucoseisletKATPlivermetabolism

Identifiers

PMID29898400
PMCPMC6581793
OpenAlexW2807927825

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.