Introduction: Measurement of pancreatic beta cell mass in animal models is a common assay in diabetes researches. Novel whole-organ clearance methods in conjunction with transgenic mouse models hold tremendous promise to improve beta cell mass measurement methods. Here, we proposed a refined method to estimate the beta cell mass using a new transgenic Tg(Pdx1-GFP) mouse model and a recently developed free-of-acrylamide clearing tissue (FACT) protocol. Methods: First, we generated and evaluated a Tg(Pdx1-GFP) transgenic mouse model. Using the FACT protocol in our model, we could quantify the beta cell mass and alloxan-induced beta cell destruction in whole pancreas specimens. Results: Compiled fluorescent images of pancreas resulted in enhanced beta cell mass characterization in FACT-cleared sections (2928869±, 120215 AU) compared to No-FACT cleared sections (1292372±, 325632 AU). Additionally, the total number of detected islets with this method was significantly higher than the other clearance methods (155. 7 and 109, respectively). Using this method, we showed green fluorescent protein (GFP) expression confined to beta cells in Tg(Pdx1-GFP) transgenic. This enhanced GFP expression enabled us to accurately measure beta cell loss in a beta cell destruction model. The results suggest that our proposed method can be used as a simple, and rapid assay for beta cell mass measurement in islet biology and diabetes studies. Conclusion: The Tg(Pdx1-GFP) transgenic mouse in conjunction with the FACT protocol can enhance large-scale screening studies in the field of diabetes.

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, TNFa) 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.