Abstract

Introduction: Gama amino butyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian nervous system. Pancreatic beta cells in islets of Langerhans express GABA at the levels comparable to those encountered in the central nervous system. The concentrations of GABA and the number of GABA secreting cells, decrease in diabetic patients and experimental diabetes models. Reports on effects of GABA on insulin secretion have been controversial. In this study we investigated whether or not GABA administration in an animal diabetes model can change insulin and glucagon secretion and improve diabetic symptoms. Materials and Methods: Seven-week old CD1 mice were used. For inducing diabetes, 40 mg/kg of streptozotocin (STZ) was given intraperitoneally for 5 days. Two months after diabetic induction, animals were divided into two groups, one receiving 200 μmol of GABA, while the other group received phosphate buffer solution (PBS) for two and half months. Results: After 42 days, the glucose concentration in the GABA treated group decreased significantly compared to the untreated group and the first day. After two and half months, water consumption in the GABA treated group decreased significantly in comparison to the control group. Plasma insulin level increased significantly (0.989±0.67 vs 0.779±0.11) while plasma glucagon level decreased significantly (91.71±4.52 vs 130.07±18.78). Glucose tolerance test in the GABA group returned to normal levels. Conclusion: GABA administration by regulation of insulin and glucagon secretion could help treat some diabetic symptoms, and could possibly be used in the future as a therapeutic tool in diabetes.