Type 1 diabetes is characterized by an increase in blood glucose levels resulting from damage to β cells in pancreatic islets and the consequent absolute insufficiency of insulin. Animal models of type 1 diabetes were usually established using drugs toxic to β cells, such as streptozotocin (STZ). To assess the application of zebrafish larvae in diabetes research, we explore the effects of STZ on pancreatic islets and glucose metabolism in zebrafish larvae. STZ was microinjected into the pericardial cavity of zebrafish larvae on alternate days for three times. At 2 days after the whole series of STZ injection (12 dpf), free-glucose level in larvae tissue shows a significant increase, and the fluorescence signal in immunohistochemistry, which indicates the insulin expression, was significantly weaker compared with the solution-injected control. Obvious apoptosis signals were also observed in the location of pancreatic islet, and insulin content decreased to be undetectable in STZ-injected larvae. Gene expression level of ins decreased to half of the solution injection control and that of casp3a was upregulated by 2.20-fold. Expression level of glut2 and gck decreased to 0.312-fold and 0.093-fold, respectively. pck1 was upregulated by 2.533-fold in STZ-injected larvae. By tracking detection, we found the free-glucose level in STZ-injected larvae gradually approached the level of the solution injection control and the insulin content recovered at 6 days post-STZ injection (16 dpf). Consistent with the change of the glucose level, the regeneration rate of the caudal fin in the STZ-injected group decreased initially, but recovered and accelerated gradually finally at 8 days post-amputation (20 dpf). These results indicate the generation of a transient hyperglycemia model due to β-cell apoptosis caused by STZ, which is abated by the vigorous regeneration ability of β cells in zebrafish larvae.

1型糖尿病的特征是由于胰岛中的β细胞受损以及由此导致的胰岛素绝对供血不足导致血糖水平升高。通常使用对β细胞有毒性的药物，例如链脲佐菌素（STZ）建立1型糖尿病的动物模型。为了评估斑马鱼幼虫在糖尿病研究中的应用，我们探讨了STZ对斑马鱼幼虫胰岛和葡萄糖代谢的影响。隔天将STZ微注射到斑马鱼幼虫的心包腔中3次。在整个系列的STZ注射（12 dpf）后第2天，幼虫组织中的游离葡萄糖水平显着增加，并且与注射溶液的对照组相比，免疫组化中指示胰岛素表达的荧光信号明显减弱。 。在胰岛的位置也观察到明显的凋亡信号，并且在注射STZ的幼虫中胰岛素含量降低至无法检测到。基因表达水平ins降低到溶液注入对照的一半，而casp3a的表达则上调2.20倍。glut2和gck的表达水平分别降至0.312倍和0.093倍。pck1被STZ注射的幼虫中的上调了2.533倍。通过跟踪检测，我们发现注射STZ的幼虫中的游离葡萄糖水平逐渐接近溶液注射对照水平，并且在STZ注射后6天（16 dpf）恢复了胰岛素含量。与葡萄糖水平的变化一致，注射STZ的组尾鳍的再生速率开始下降，但在截肢后第8天（20 dpf）逐渐恢复并逐渐加速。这些结果表明，由于STZ引起的β细胞凋亡导致了短暂性高血糖模型的产生，而斑马鱼幼虫中β细胞的旺盛再生能力减弱了这种模型。