There is considerable evidence that the gastrointestinal hormone cholecystokinin (CCK) induces satiety and reduces food intake in both animals and humans. Impaired CCK secretion was recently reported in patients with bulimia nervosa (BN) in whom plasma CCK responses to a standardized mixed-liquid meal were significantly lower than in controls. The present study was undertaken to determine whether CCK levels were abnormal in another relatively common eating disorder, anorexia nervosa (AN), before and after therapy and to investigate the relationship to the abnormal eating behavior. Plasma CCK, serum glucose, and immunoreactive insulin (IRI) responses to a 50-g oral glucose load were measured in 13 women with AN and in nine normal sex- and age-matched controls. The AN patients were all hospitalized during treatment; following partial restoration of body weight, the tests were repeated. Initial body weights were 70.8% ± 1.8% (mean ± SEM) of ideal body weight (IBW), and following partial restoration were 84.3% ± 1.4%. Body weights in normal controls were 96.3% ± 2.1% of IBW. Initial basal CCK concentrations in the AN patients before nutritional and cognitive behavioral therapy were significantly greater than those in controls ( P < .01). After partial restoration of body weight, basal CCK concentration in AN patients approached that of control subjects. When AN patients were given a glucose load before therapy, the change in CCK response was diminished when compared with that of controls. However, CCK responses to the glucose load in AN patients following therapy were similar to those of controls. Blood glucose levels following the oral glucose load were essentially the same as those observed in the controls; however, changes in levels of IRI following the glucose load in AN patients before and after treatment were significantly less than those in the controls. These data indicate that basal CCK levels are abnormally elevated in AN patients, and that diminished responses to an oral glucose load are essentially normalized after therapy and partial restoration of body weight. The significance of the elevated basal CCK levels in AN remains to be elucidated.