Evidence map›Paper›PMID 19073765›Full record

ArticleDiabetes2009

Mitochondrial reactive oxygen species are obligatory signals for glucose-induced insulin secretion.

Corinne Leloup, Cécile Tourrel-Cuzin, Christophe Magnan, Melis Karaca, Julien Castel, Lionel Carneiro, Anne-Laure Colombani, Alain Ktorza, Louis Casteilla, Luc Pénicaud

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed
19.6field-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

183 citing papers in PubMed, 356 citations in OpenAlex.

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  10. New Insight Into Male Infertility: Deviation From Basic Tenets of Life.Oxidative medicine and cellular longevity · 2026
    Review
  11. Article
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  13. Mechanosensitive Channels Mediate Pancreatic β Cells Reactive Oxygen Species Formation and Downregulation of Essential Genes During Therapeutic Ultrasound Treatment.Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine · 2025
    Article
  14. Review
  15. IFN-α Induces Heterogenous ROS Production in Human β-Cells.bioRxiv : the preprint server for biology · 2025
    Article
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123 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

10 authors at 1 institution in 1 country.

Corinne LeloupDepartment of Metabolism, Plasticity, and Mitochondria, Unité Mixte de Recherche 5241, Centre National de la Recherche Scientifique-Université Paul Sabatier, Institut Fédératif de Recherche 31, Toulouse, France. coleloup@toulouse.inserm.fr
Cécile Tourrel-Cuzin
Christophe Magnan
Melis Karaca
Julien Castel
Lionel Carneiro
Anne-Laure Colombani
Alain Ktorza
Louis Casteilla
Luc Pénicaud
Université Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveInsulin secretion involves complex events in which the mitochondria play a pivotal role in the generation of signals that couple glucose detection to insulin secretion. Studies on the mitochondrial generation of reactive oxygen species (ROS) generally focus on chronic nutrient exposure. Here, we investigate whether transient mitochondrial ROS production linked to glucose-induced increased respiration might act as a signal for monitoring insulin secretion. RESEARCH DESIGN AND

methodsROS production in response to glucose was investigated in freshly isolated rat islets. ROS effects were studied using a pharmacological approach and calcium imaging.

resultsTransient glucose increase from 5.5 to 16.7 mmol/l stimulated ROS generation, which was reversed by antioxidants. Insulin secretion was dose dependently blunted by antioxidants and highly correlated with ROS levels. The incapacity of beta-cells to secrete insulin in response to glucose with antioxidants was associated with a decrease in ROS production and in contrast to the maintenance of high levels of ATP and NADH. Then, we investigated the mitochondrial origin of ROS (mROS) as the triggering signal. Insulin release was mimicked by the mitochondrial-complex blockers, antimycin and rotenone, that generate mROS. The adding of antioxidants to mitochondrial blockers or to glucose was used to lower mROS reversed insulin secretion. Finally, calcium imaging on perifused islets using glucose stimulation or mitochondrial blockers revealed that calcium mobilization was completely reversed using the antioxidant trolox and that it was of extracellular origin. No toxic effects were present using these pharmacological approaches.

conclusionsAltogether, these complementary results demonstrate that mROS production is a necessary stimulus for glucose-induced insulin secretion.

Indexed as

Adenosine TriphosphateAnimalsCalciumChromansGlucoseInsulinInsulin SecretionIslets of LangerhansKineticsMaleMitochondriaNADRatsRats, WistarReactive Oxygen SpeciesSignal Transduction6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acidAdenosine TriphosphateCalciumChromansGlucoseInsulinNADReactive Oxygen SpeciesSuperoxide DismutaseSuperoxidesThapsigargin

Identifiers

PMID19073765
PMCPMC2646066
OpenAlexW2128342607

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.