Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of voltage-gated calcium channels. Calcium enters the cell and triggers the docking, priming, and fusion of the insulin secretory vesicles with the plasma membrane for insulin release.

Insulin secretory vesicles follow the "kiss-and-run" model of exocytosis. In this model, when a secretory vesicle fuses with the plasma membrane, it opens a fusion pore to release insulin, closes the pore, and returns to the cytoplasm. The released insulin stimulates glucose uptake by cells and suppresses gluconeogenesis– new glucose formation by the liver.

Hormonal and neuronal signals regulate insulin secretion from β-islet cells. Molecules regulating insulin secretion include epinephrine, acetylcholine, and somatostatin. Defects in the biogenesis of insulin secretory vesicles, their fusion with the plasma membrane, or the exocytosis of insulin can lead to diabetes mellitus.