Pancreatic cells secrete insulin in response to a "sensing" mechanism triggered by an increase in glucose from basal levels. Stimulation-secretion coupling in cells is different from other cell types because instead of being mediated by receptor binding, glucose needs to be transported into the cytoplasm and metabolized in order to stimulate exocytosis. Previous reviews (Schuit et al. 2001; MacDonald et al. 2005) have divided the glucose sensing apparatus into proximal metabolic and distal ionic apparatus. The proximal component includes glucose transport through a specific transporter on the cell membrane (Glut 1 for humans, Glut2 for rodents) followed by the glycolytic pathway, which results in changes in the ATP/ADP ratio that trigger the distal component comprised by a cascade of electrochemical events, that culminate in an increase in intracellular calcium (Ca²⁺)_i and stimulation of insulin secretion. This process can be augmented by several entero-insular hormones (GLP-1, GIP and CCK) and neurotransmitters like acetylcholine which amplify the secretory response through the activation of adenylate cyclase or phospholipase C.