Barakat Hassan, Aljutaily Thamer
Department of Food Science and Human Nutrition, College of Agriculture and Food, Qassim University, Buraydah 51452, Saudi Arabia.
Biomolecules. 2025 Mar 11;15(3):399. doi: 10.3390/biom15030399.
GABA (γ-Aminobutyric Acid), a well-established inhibitory neurotransmitter in the central nervous system, has garnered considerable interest for its potential role in diabetes management, particularly due to its presence in pancreatic islets. This review aims to explore the therapeutic role of GABA in diabetes management and its potential mechanisms for antidiabetic effects. Relevant studies were searched across databases such as PubMed and ScienceDirect, applying strict eligibility criteria focused on GABA administration methods and diabetic models. The collective results showed that the administration of GABA in diabetic models resulted in remarkable enhancements in glucose and insulin homeostasis, favorable modifications in lipid profiles, and amelioration of dysfunctions across neural, hepatic, renal, and cardiac systems. The findings from the literature demonstrated that GABAergic signaling within pancreatic tissues can significantly contribute to the stimulation of β cell proliferation through the facilitation of a sustained -differentiation process, wherein glucagon-secreting α cells are converted into insulin-secreting β-like cells. In addition, activated GABAergic signaling can trigger the initiation of the PI3K/AKT signaling pathway within pancreatic tissues, leading to improved insulin signaling and maintained glucose homeostasis. GABAergic signaling can further function within hepatic tissues, promoting inhibitory effects on the expression of genes related to gluconeogenesis and lipogenesis. Moreover, GABA may enhance gut microbiota diversity by attenuating gut inflammation, attributable to its anti-inflammatory and immunomodulatory properties. Furthermore, the neuroprotective effects of GABA play a significant role in ameliorating neural disorders associated with diabetes by facilitating a substantial reduction in neuronal apoptosis. In conclusion, GABA emerges as a promising candidate for an antidiabetic agent; however, further research is highly encouraged to develop a rigorously designed framework that comprehensively identifies and optimizes the appropriate dosages and intervention methods for effectively managing and combating diabetes.
γ-氨基丁酸（GABA）是中枢神经系统中一种公认的抑制性神经递质，因其在糖尿病管理中的潜在作用而备受关注，尤其是它存在于胰岛中。本综述旨在探讨GABA在糖尿病管理中的治疗作用及其抗糖尿病作用的潜在机制。在PubMed和ScienceDirect等数据库中检索了相关研究，应用严格的纳入标准，重点关注GABA给药方法和糖尿病模型。综合结果表明，在糖尿病模型中给予GABA可显著改善葡萄糖和胰岛素稳态，改善脂质谱，并改善神经、肝脏、肾脏和心脏系统的功能障碍。文献研究结果表明，胰腺组织内的GABA能信号可通过促进持续分化过程，显著促进β细胞增殖，在此过程中，分泌胰高血糖素的α细胞转化为分泌胰岛素的β样细胞。此外，激活的GABA能信号可触发胰腺组织内PI3K/AKT信号通路的启动，从而改善胰岛素信号并维持葡萄糖稳态。GABA能信号还可在肝脏组织中发挥作用，对糖异生和脂肪生成相关基因的表达产生抑制作用。此外，GABA可通过减轻肠道炎症来增强肠道微生物群多样性，这归因于其抗炎和免疫调节特性。此外，GABA的神经保护作用通过促进神经元凋亡的显著减少，在改善与糖尿病相关的神经障碍方面发挥重要作用。总之，GABA有望成为一种抗糖尿病药物；然而，强烈鼓励进一步开展研究，以建立一个设计严谨的框架，全面确定并优化有效管理和对抗糖尿病的合适剂量和干预方法。
