Evaluation of mitochondrial divisions in mouse with type‐2 diabetes and effect of glucose‐oxidase on mouse islet cells RIN‐m5F

Abstract

To elucidate the relationship between dynamic variations of insular β cell mitochondria and type-2 diabetes by using a mouse model, the dynamic variation (fusion or fission) of insular β cell mitochondria present in two groups of Wistar mice with type-2 diabetes (high fat feeding and streptozotocin (STZ) adding with low dose and high frequency, high fat feeding and STZ adding with high dose and low frequency), and normal Wistar mouse were systematically compared. By analysing the insulin secretion level and other related indexes, the molecular mechanism of the fusion or fission phenomenon of insular β cell mitochondria in two different models (high fat feeding and STZ adding with low dose and high frequency, high fat feeding and STZ adding with high dose and low frequency) of mice with type-2 diabetes were initially elucidated. The phenomenon of mitochondrial fusion and fission was clearly seen. In initially determining the relationship between the change of insular β cell mitochondrial structure and its cell apoptosis generated by some factors such as treatment by glucose-oxidase (GO), the effect of GO on the mouse islet cells RIN-m5F including the effects on cell growth, reactive oxygen species (ROS), cell cycle, cell apoptosis of RIN-m5F were systematically examined. GO showed some influence on the mouse islet cells RIN-m5F cell activity, ROS and apoptosis, but its effect on the cell cycle was not significant.