Increases in blood glucose stimulate pancreatic beta-islet cells to synthesize proinsulin, an insulin precursor. Newly synthesized proinsulin enters the trans-Golgi network, where it is present in a diffuse form inside immature secretory vesicles. As the vesicles fuse together and mature, enzymes cleave proinsulin to form active insulin, which concentrates inside the vesicles, forming dense core vesicles. High blood glucose also causes a glucose-induced calcium influx through a calcium channel. Calcium triggers a signaling cascade that eventually activates protein kinase C or PKC. PKC enables reorganization of the actin network inside the cell to translocate the insulin containing secretory vesicles. The secretory vesicle then fuses with the plasma membrane to release large amounts of insulin in response to the increased blood glucose.