Cholecystokinin And Satiety

Peripheral or central administration of the brain/gut peptide cholecystokinin (CCK) inhibits food intake. The actions of peripheral CCK in feeding are consistent with a role in satiety. CCK has been shown to effectively reduce food intake in birds, rodents, pigs, sheep, nonhuman primates, and humans. CCK affects both solid and liquid food intake and is effective in spontaneous food intake as well as feeding that is stimulated by access to a palatable food source or in response to deprivation. CCK is rapidly released during a meal, exogenous peptide terminates an individual meal without long-term effects on food intake, and CCK antagonists or genetic manipulations that alter CCK-A receptor signaling result in increases in meal size. A role for central CCK in energy balance is suggested from the ability of central CCK to inhibit food intake and the gene-expression changes underlying the hyperphagia and obesity of Otsuka Long Evans Tokushima Fatty (OLETF) rats lacking CCK-A receptors. Alterations in CCK-A receptor signaling have recently been implicated in human obesity.