These studies, therefore, allow a model of how CCK and insulin regulate the acinar pancreas in a coordinated manner (Fig. 27). CCK, after its secretion by gut cells, interacts with a specific receptor on the cell surface and then increases intracellular free Ca2+. Ca2+, in turn (1) interacts with the secretory granules leading to zymogen release, (2) stimulates protein synthesis, and (3) increases glucose transport. The model is supported on the finding of specific high affinity CCK receptors on acini and by the localization of CCK to the plasma membrane in EM autoradiographs. Insulin, secreted from the pancreatic islets, also interacts with a specific receptor on the cell surface. Either via a messenger generated by this reaction, or via insulin's subsequent direct interaction with intracellular organelles, such as the Golgi-endoplasmic reticulum, protein synthesis is initiated and glucose transport is increased. Then a series of events is initiated to increase cell growth, amylase content, and sensitivity to CCK. These studies, therefore, indicate that the control of acinar cell function is a product of cooperative intrahormonal interactions.