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Cited by 100Pancreatic function and diabetesDiabetes Treatment and ManagementDiabetes and associated disorders

GABAergic system in the endocrine pancreas: a new target for diabetes treatment

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Wang, Qinghua, Prud'homme, Gerald, Wan, Yun·2015·Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
DOI 10.2147/dmso.s50642PMC PMC4322886
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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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  • Activation of GABA receptors leads to Ca2+-influx stimulating or activation of PI3K/Akt/PKB pathway resulting in increased insulin release, promotes pancreatic β-cell proliferation, and inhibits apoptosis.

    “Pancreas β-cells express gamma amino butyric acid receptor A/B (GABAA/BRs) and activation of GABA receptors leads to Ca2+-influx stimulating or activation of PI3K/Akt/PKB pathway resulting in increased insulin release promotes pancreatic β-cells proliferation and inhibits apoptosis.”

    From A critical review on diabetes mellitus type 1 and type 2 management approaches: from lifestyle modification to current and novel targets and therapeutic agents. (2024) · cites this paper as [103]

    The β-Cells subsection of “Signaling mechanisms of GABA action” reports GABA-associated calcium signaling and Akt activation that promote β-cell proliferation and survival; the preclinical-therapy section also reports decreased apoptosis. But the paper does not establish that this pathway increases insulin release: its signaling discussion says GABAB-receptor activation can inhibit insulin secretion at high glucose levels, and describes GABAB-mediated CREB activation as independent of PI3K/Akt. Page numbers are unavailable in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • GABA regulates both the survival and regeneration of human pancreatic β-cells.

    “Thus, GABA regulates both the survival and regeneration of human pancreatic β-cells.”

    From A critical review on diabetes mellitus type 1 and type 2 management approaches: from lifestyle modification to current and novel targets and therapeutic agents. (2024) · cites this paper as [103]

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Authors
Wang, Q., Prud'homme, G., & Wan, Y.
Affiliations
  • St. Michael's Hospital (CA)
  • Shanghai Medical College of Fudan University (CN)
Corresponding author
Wang, Qinghua
ORCID
Wang, Qinghua
Venue
Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
Publisher
Informa UK Limited
Published
2015-02
Volume
8
Pages
79
ISSN
1178-7007 (ISSN-L)
DOI
10.2147/dmso.s50642
PMC
PMC4322886
OpenAlex
W2101460751
Cited by
100
References
5
Citations by year
2026: 1 · 2025: 12 · 2024: 11 · 2023: 6 · 2022: 12 · 2021: 14 · 2020: 10 · 2019: 9 · 2018: 9 · 2017: 7 · 2016: 4 · 2015: 5
FWCI
1.60
Type
journal article
Language
en
Open access
Licence
Locations
  • Diabetes Metabolic Syndrome and Obesity (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
Funders
  • National Science Foundation
  • Canadian Diabetes Association
  • National Natural Science Foundation of China
  • Canadian Institutes of Health Research
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords
GABA, pancreatic beta cells, beta cell regeneration, beta-cell apoptosis, type 1 diabetes, type 2 diabetes, insulitis, anti-inflammatory activity, immune regulation, GABA signaling, diabetes treatment

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