Evidence map›Paper›PMID 22538358›Full record

ArticleDiabetologia2012

γ-Aminobutyric acid (GABA) signalling in human pancreatic islets is altered in type 2 diabetes.

J Taneera, Z Jin, Y Jin, S J Muhammed, E Zhang, S Lang, A Salehi, O Korsgren, E Renström, L Groop and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
10.3field-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

64 citing papers in PubMed, 115 citations in OpenAlex.

  1. Peripheral GABA Signaling in Metabolic Adaptation and Maladaptation.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. PET imaging of GABAEJNMMI research · 2024
    Article
  9. Review
  10. Article
  11. The role of GABA in type 1 diabetes.Frontiers in endocrinology · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. GABA signalling in human pancreatic islets.Frontiers in endocrinology · 2023
    Review
  16. The relationship between GAD65 autoantibody and the risk of T1DM onset.Journal of diabetes and metabolic disorders · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Combination Therapy with GABA and MgSOInternational journal of endocrinology · 2022
    Article

4 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

11 authors at 2 institutions in 1 country.

J TaneeraDepartment of Clinical Sciences, Lund University Diabetes Center, University Hospital Malmö, Lund University, Malmö, Sweden.
Z Jin
Y Jin
S J Muhammed
E Zhang
S Lang
A Salehi
O Korsgren
E Renström
L Groop
B Birnir
Lund University · SEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisγ-Aminobutyric acid (GABA) is a signalling molecule in the interstitial space in pancreatic islets. We examined the expression and function of the GABA signalling system components in human pancreatic islets from normoglycaemic and type 2 diabetic individuals.

methodsExpression of GABA signalling system components was studied by microarray, quantitative PCR analysis, immunohistochemistry and patch-clamp experiments on cells in intact islets. Hormone release was measured from intact islets.

resultsThe GABA signalling system was compromised in islets from type 2 diabetic individuals, where the expression of the genes encoding the α1, α2, β2 and β3 GABA(A) channel subunits was downregulated. GABA originating within the islets evoked tonic currents in the cells. The currents were enhanced by pentobarbital and inhibited by the GABA(A) receptor antagonist, SR95531. The effects of SR95531 on hormone release revealed that activation of GABA(A) channels (GABA(A) receptors) decreased both insulin and glucagon secretion. The GABA(B) receptor antagonist, CPG55845, increased insulin release in islets (16.7 mmol/l glucose) from normoglycaemic and type 2 diabetic individuals. CONCLUSIONS/

interpretationInterstitial GABA activates GABA(A) channels and GABA(B) receptors and effectively modulates hormone release in islets from type 2 diabetic and normoglycaemic individuals.

Indexed as

Diabetes Mellitus, Type 2Disease ProgressionDose-Response Relationship, DrugDown-RegulationFemaleGABA Antagonistsgamma-Aminobutyric AcidHomeostasisHumansImmunohistochemistryInsulin-Secreting CellsMaleMiddle AgedPyridazinesReceptors, GABA-BSignal TransductionGABA Antagonistsgabazinegamma-Aminobutyric AcidPyridazinesReceptors, GABA-B

Identifiers

PMID22538358
PMCPMC3369140
OpenAlexW1977392097

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.