This article has centered on the hormonal actions of CCK on a variety of different target tissues. Until the development of specific assays for measuring plasma levels of the hormone, it was not possible to distinguish physiologic from pharmacologic effects. However, by the methods described earlier it now has become clear that CCK, in physiologic concentrations, stimulates gallbladder contraction, delays gastric emptying, potentiates insulin secretion, and may affect satiety. Actions of CCK that have been studied by radioimmunoassay methods and determined also to be physiologic include stimulation of pancreatic exocrine secretion. Other actions of CCK that may be physiologic but have not been thoroughly investigated include effects on bowel motility, relaxation of lower esophageal sphincter pressure, regulation of sphincter of Oddi pressure, effects on analgesia, and modification of behavior. Some of these actions may be attributable to endogenous, but neurally released CCK and, therefore, would not be hormonal actions. However, continued investigations with specific CCK receptor antagonists together with accurate measurements of circulating levels of CCK should make it possible to define the physiologic importance of CCK on these other potential sites of action. The variety of CCK's physiologic effects emphasizes its integrative function on both digestive and metabolic processes. After a meal, in a highly coordinated fashion, CCK (1) regulates the movement of nutrients through the gastrointestinal tract, (2) contracts the gallbladder and stimulates pancreatic exocrine secretion to facilitate digestion, and (3) potentiates amino acid-induced insulin secretion and delays gastric emptying to maintain euglycemia. An effect to reduce food intake following food ingestion would be a logical extension of these integrated actions. Thus, CCK appears to have an essential role in regulating the intake, processing, and distribution of essential nutrients.