Evidence map›Paper›PMID 21709230›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

GABA exerts protective and regenerative effects on islet beta cells and reverses diabetes.

Nepton Soltani, Hongmin Qiu, Mila Aleksic, Yelena Glinka, Fang Zhao, Rui Liu, Yiming Li, Nina Zhang, Rabindranath Chakrabarti, Tiffany Ng and 6 more

2 registry-linked trialsAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 206 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed, 1 pooled it
20.0field-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.

NCT02002130 phase1completednot on this mapstarted 2015, after this paper: background citation

The Use of Glutamic Acid Decarboxylase (GAD)and Gamma-Amino Butyric Acid(GABA)in the Treatment of Type I Diabetes.

TypeinterventionalSponsorUniversity of Alabama at BirminghamRan2015 to 2022Enrolled101ConditionsType I DiabetesArmsPlacebo GABA and Placebo GAD-alum, GABA and Placebo GAD-alum, Active Oral GABA and Active GAD-alum injection
NCT05905393 phase3unknown statusnot on this mapstarted 2023, after this paper: background citation

The Protective Role of Preoperative Stimulation of the Distal Limb of the Ileostomy Loop With GABA Before Ileostomy Closure

TypeinterventionalSponsorQilu Hospital of Shandong UniversityRan2023 to 2024Enrolled80ConditionsIleostomy, ComplicationsArmspreoperative stimulation of the efferent loop with GABA before ileostomy closure surgery, preoperative stimulation of the efferent loop with only physiological saline
3 · Its place in the literature

Who cites it

206 citing papers in PubMed, 1 synthesis or guideline pooled it, 405 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Peripheral GABA Signaling in Metabolic Adaptation and Maladaptation.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Review
  10. GABA Regulates CaMetabolites · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Exploring the mechanisms connecting the sympathetic nervous system and type 2 diabetes: Focus on renal denervation.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2026
    Review
  18. Article
  19. Review
  20. Article

146 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

16 authors at 5 institutions in 3 countries.

Nepton SoltaniDivision of Endocrinology and Metabolism, the Keenan Research Centre in the Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON, Canada M5B 1W8.
Hongmin Qiu
Mila Aleksic
Yelena Glinka
Fang Zhao
Rui Liu
Yiming Li
Nina Zhang
Rabindranath Chakrabarti
Tiffany Ng
Tianru Jin
Haibo Zhang
Wei-Yang Lu
Zhong-Ping Feng
Gerald J Prud'homme
Qinghua Wang
University of Toronto · CASt. Michael's Hospital · CAFudan University · CNHuashan Hospital · CNWestern University · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disease characterized by insulitis and islet β-cell loss. Thus, an effective therapy may require β-cell restoration and immune suppression. Currently, there is no treatment that can achieve both goals efficiently. We report here that GABA exerts antidiabetic effects by acting on both the islet β-cells and immune system. Unlike in adult brain or islet α-cells in which GABA exerts hyperpolarizing effects, in islet β-cells, GABA produces membrane depolarization and Ca(2+) influx, leading to the activation of PI3-K/Akt-dependent growth and survival pathways. This provides a potential mechanism underlying our in vivo findings that GABA therapy preserves β-cell mass and prevents the development of T1D. Remarkably, in severely diabetic mice, GABA restores β-cell mass and reverses the disease. Furthermore, GABA suppresses insulitis and systemic inflammatory cytokine production. The β-cell regenerative and immunoinhibitory effects of GABA provide insights into the role of GABA in regulating islet cell function and glucose homeostasis, which may find clinical application.

Indexed as

AnimalsApoptosisCalcium SignalingCell ProliferationCytokinesDiabetes Mellitus, Type 1Femalegamma-Aminobutyric AcidHyperglycemiaImmunosuppressive AgentsInflammation MediatorsInsulin-Secreting CellsMaleMembrane PotentialsMiceMice, Inbred NODCytokinesgamma-Aminobutyric AcidImmunosuppressive AgentsInflammation MediatorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID21709230
PMCPMC3136292
OpenAlexW2050397606

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.