Cholecystokinin in obesity and other disorders of eating

Animal and human studies have examined aspects of the physiology of cholecystokinin (CCK) under a variety of metabolic circumstances. The absence of CCK or the CCK1 receptor results in alterations in meal patterns and, in some conditions, overeating and obesity. Sensitivity to the feeding inhibitory actions of CCK has been shown to be affected by metabolic status in rodent studies. In contrast, responsiveness to exogenous CCK is maintained with obesity in human studies. Both basal and meal-stimulated plasma levels of CCK are differentially affected across a range of eating disorders. Responsivity to CCK has been assessed in some but not all eating disorders. With the exception of the anorexia of aging, altered CCK physiology is likely a result of disordered eating rather than a causal factor.