Abstract

Introduction: Type I diabetes is an autoimmune disease associated with T lymphocytes function in beta cells. This process can increase cytokine secretion, which can cause beta cell inflammation and death. Since GABA, (γ-aminobutyric acid) is a major inhibitory neurotransmitter, and low concentration of GABA can increase cytokine secretion, the aim of this study was demonstrate to the inhibitory effect of GABA administration on cytokine secretion and decrease in beta cell death and also to show the ability of beta cells in insulin secretion. Material and Methods: Seven week old CD1 mice were used. To induce diabetes, animals received 40 mg/kg of STZ five days continuously. Two months later, animals were divided into two groups, one receiving 200 micromole of GABA and the other (controls) the same volume of PBS for 10 weeks. Results: Serum glucagon levels, and alpha cells significantly decreased in the (IL12 IL1β, TNFα) mass and some cytokine levels in the GABA group. Plasma insulin level and beta cell mass significantly increased in comparison to the control group. Conclusion: From the results of this study we conclude that GABA administration causes inhibition in cytokine secretion, improves beta cell mass and increases insulin secretion. May be, in the future, if GABA shows no side effects we can use GABA for type one diabetes.