Fig. 1. Glucose-stimulated insulin secretion (GSIS) from pancreatic β-cells. Upon uptake into the pancreatic β-cell, glucose is metabolized into ATP. The rising ATP/ADP ratio inhibits K_ATP which causes membrane depolarization and the opening of Ca_v. The resulting increased [Ca²⁺]_i triggers the fusion of secretory granules and the release of insulin. K_v channels work to repolarize the cell, generating oscillations in [Ca²⁺]_i. GPR40 stimulation also leads to increased [Ca²⁺]_i, further potentiating GSIS.