Evidence map›Paper›PMID 21335552›Full record

ArticleThe Journal of biological chemistry2011

The glial glutamate transporter 1 (GLT1) is expressed by pancreatic beta-cells and prevents glutamate-induced beta-cell death.

Eliana S Di Cairano, Alberto M Davalli, Lucia Perego, Silvia Sala, V Franca Sacchi, Stefano La Rosa, Giovanna Finzi, Claudia Placidi, Carlo Capella, Paola Conti and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 68 citations in OpenAlex.

  1. Trial
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  7. Mechanisms of action of incretin receptor based dual- and tri-agonists in pancreatic islets.American journal of physiology. Endocrinology and metabolism · 2023
    Review
  8. Article
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  11. Article
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  17. Metabolomics of Type 1 and Type 2 Diabetes.International journal of molecular sciences · 2019
    Review
  18. Article
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  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 3 countries.

Eliana S Di CairanoDepartment of Molecular Science Applied to Biosystems, Università degli Studi di Milano, 20134 Milan, Italy.
Alberto M Davalli
Lucia Perego
Silvia Sala
V Franca Sacchi
Stefano La Rosa
Giovanna Finzi
Claudia Placidi
Carlo Capella
Paola Conti
Victoria E Centonze
Francesca Casiraghi
Federico Bertuzzi
Franco Folli
Carla Perego
University of Milan · ITUniversity of Insubria · ITDiabetes Australia · AUAzienda Socio Sanitaria Territoriale Grande Ospedale Metropolitano Niguarda · ITThe University of Texas Health Science Center at San Antonio · US

Funding

Beta Cell Adaptation to Stress in Baboon Pancreas After Partial PancreatectomyR01DK080148 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FOLLI, FRANCO BATTISTA ENNIO · 2009 to 2010
$897k
NIDDK NIH HHS R01 DK080148
6 · The paper itself

Abstract

Glutamate is the major excitatory neurotransmitter of the central nervous system (CNS) and may induce cytotoxicity through persistent activation of glutamate receptors and oxidative stress. Its extracellular concentration is maintained at physiological concentrations by high affinity glutamate transporters of the solute carrier 1 family (SLC1). Glutamate is also present in islet of Langerhans where it is secreted by the α-cells and acts as a signaling molecule to modulate hormone secretion. Whether glutamate plays a role in islet cell viability is presently unknown. We demonstrate that chronic exposure to glutamate exerts a cytotoxic effect in clonal β-cell lines and human islet β-cells but not in α-cells. In human islets, glutamate-induced β-cell cytotoxicity was associated with increased oxidative stress and led to apoptosis and autophagy. We also provide evidence that the key regulator of extracellular islet glutamate concentration is the glial glutamate transporter 1 (GLT1). GLT1 localizes to the plasma membrane of β-cells, modulates hormone secretion, and prevents glutamate-induced cytotoxicity as shown by the fact that its down-regulation induced β-cell death, whereas GLT1 up-regulation promoted β-cell survival. In conclusion, the present study identifies GLT1 as a new player in glutamate homeostasis and signaling in the islet of Langerhans and demonstrates that β-cells critically depend on its activity to control extracellular glutamate levels and cellular integrity.

Indexed as

Gene Expression RegulationAnimalsApoptosisAutophagyCell SurvivalExcitatory Amino Acid Transporter 2Glutamate Plasma Membrane Transport ProteinsGlutamic AcidHomeostasisHumansInsulin-Secreting CellsIslets of LangerhansMiceModels, BiologicalOxidative StressExcitatory Amino Acid Transporter 2Glutamate Plasma Membrane Transport ProteinsGlutamic AcidSLC1A2 protein, humanSlc1a2 protein, mouse

Identifiers

PMID21335552
PMCPMC3077601
OpenAlexW2010387488

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.