ReviewDiabetes, metabolic syndrome and obesity : targets and therapy2015
GABAergic system in the endocrine pancreas: a new target for diabetes treatment.
Review in Diabetes, metabolic syndrome and obesity : targets and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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.
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.
Who cites it
50 citing papers in PubMed, 99 citations in OpenAlex.
- Trial
- GABA as an Overlooked Mediator of Metformin Action: GABA-mediated Neuropsychiatric and Hepatoprotective Activities of Metformin.Annals of neurosciences · 2026Review
- Markers Predicting Cure With Combinatorial Treatment in a Mouse Model of Latent Autoimmune Diabetes in Adults.MedComm · 2026Article
- GABA Enhances Growth Hormone Expression by Modulating Somatotroph Pit-1 Transcription via Activation of Calmodulin-Dependent Kinases.Nutrients · 2026Article
- The effect(s) of berberine fromIranian journal of basic medical sciences · 2026Article
- Mitochondrial DNA copy number reduction viaEpigenomics · 2026Article
- Characterization ofFoods (Basel, Switzerland) · 2025Article
- Neurotransmitter Alterations in Prediabetes and Type 2 Diabetes Mellitus: A Narrative Review.International journal of molecular sciences · 2025Review
- Microbiota-Gut-Brain Axis and Impaired Satiety in Individuals with Obesity: A Potentially Bidirectional Association.Current nutrition reports · 2025Review
- Article
- ProbioticCurrent research in food science · 2025Article
- Hyperglycemia impairs EAAT2 glutamate transporter trafficking and glutamate clearance in islets of Langerhans: implications for type 2 diabetes pathogenesis and treatment.American journal of physiology. Endocrinology and metabolism · 2024Article
- Gamma-aminobutyric acid for delaying type 1 diabetes mellitus: an update.Annals of pediatric endocrinology & metabolism · 2024Article
- A network of transcriptomic signatures identifies novel comorbidity mechanisms between schizophrenia and somatic disorders.Discover mental health · 2024Article
- Gamma-aminobutyric acid as a potential postbiotic mediator in the gut-brain axis.NPJ science of food · 2024Review
- A critical review on diabetes mellitus type 1 and type 2 management approaches: from lifestyle modification to current and novel targets and therapeutic agents.Frontiers in endocrinology · 2024Review
- The role of GABA in type 1 diabetes.Frontiers in endocrinology · 2024Review
- Genes with epigenetic alterations in human pancreatic islets impact mitochondrial function, insulin secretion, and type 2 diabetes.Nature communications · 2023Article
- Article
- Efficacy of combination therapy with GABA, a DPP-4i and a PPI as an adjunct to insulin therapy in patients with type 1 diabetes.Frontiers in endocrinology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive loss of functional pancreatic β-cell mass, mainly due to apoptosis, is a major factor in the development of hyperglycemia in both type 1 and type 2 diabetes (T1D and T2D). In T1D, β-cells are destroyed by immunological mechanisms. In T2D, while metabolic factors are known to contribute to β-cell failure and subsequent apoptosis, mounting evidence suggests that islet inflammation also plays an important role in the loss of β-cell mass. Therefore, it is of great importance for clinical intervention to develop new therapies. γ-Aminobutyric acid (GABA), a major neurotransmitter, is also produced by islet β-cells, where it functions as an important intraislet transmitter in regulating islet-cell secretion and function. Importantly, recent studies performed in rodents, including in vivo studies of xenotransplanted human islets, reveal that GABA exerts β-cell regenerative effects. Moreover, it protects β-cells against apoptosis induced by cytokines, drugs, and other stresses, and has anti-inflammatory and immunoregulatory activities. It ameliorates the manifestations of diabetes in preclinical models, suggesting potential applications for the treatment of diabetic patients. This review outlines the actions of GABA relevant to β-cell regeneration, including its signaling mechanisms and potential interactions with other mediators. These studies increase our understanding of the regenerative processes of pancreatic β-cells, and help pave the way for the development of regenerative medicine for diabetes.
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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.