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Year : 2021  |  Volume : 12  |  Issue : 1  |  Page : 19

The potential role of pancreatic γ-aminobutyric acid (GABA) in diabetes mellitus: A critical reappraisal

Department of Pharmacology, Toxicology, and Medicine, College of Medicine Almustansiriya University, P.O. Box 14132, Baghdad, Iraq

Correspondence Address:
Hayder M Al-Kuraishy
Department of Pharmacology, Toxicology, and Medicine, College of Medicine Almustansiriya University, P.O. Box 14132, Baghdad
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpvm.IJPVM_278_19

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Background: Diabetes mellitus (DM) is an endocrine disorder characterized by hyperglycemia, polyuria, polydipsia, and glucosuria. γ-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the central nervous system (CNS) of humans and other mammals. GABA acts on two different receptors, which are GABA-A and GABA-B. Pancreatic β-cells synthesize GABA from glutamic acid by glutamic acid decarboxylase (GAD). Aim: The objective of this study was to explore the potential role of pancreatic GABA on glycemic indices in DM. Methods: Evidence from experimental, preclinical, and clinical studies are evaluated for bidirectional relationships between pancreatic GABA and blood glucose disorders. A multiplicity of search strategies took on and assumed included electronic database searches of Medline and Pubmed using MeSH terms, keywords and title words during the search. Results: The pancreatic GABA signaling system has a role in the regulation of pancreatic hormone secretions, inhibition of immune response, improve β-cells survival, and change α cell into β-cell. Moreover, a GABA agonist improves the antidiabetic effects of metformin. In addition, benzodiazepine receptor agonists improve pancreatic β-cell functions through GABA dependent pathway or through modulation of pancreatic adenosine and glucagon-like peptide (GLP-1). Conclusions: Pancreatic GABA improves islet cell function, glucose homeostasis, and autoimmunity in DM. Orally administered GABA is safe for humans, and acts on peripheral GABA receptors and represents a new therapeutic modality for both T1DM and T2DM. Besides, GABA-A receptor agonist like benzodiazepines improves pancreatic β-cell function and insulin sensitivity through activation of GABA-A receptors.

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