In comparison with a saline infusion, the infusion of the C-terminal octapeptide of cholecystokinin (4 ng/kg/min) decreased food intake by an average of 122 g in a group of 12 lean men without objective evidence of untoward side effects. Shapes of the cumulative intake curves under the two conditions were similar, but subjects ate less and stopped eating sooner when receiving octapeptide than when receiving saline. These results are consistent with the hypothesis that cholecystokinin is an endogenous signal for postprandial satiety. The results offer promise for the possible use of the octapeptide as an appetite suppressant.

We studied food selection and intake of 19 women [body mass index (in kg/m2) > 30] [corrected], 10 of whom met proposed DSM-IV criteria for binge-eating disorder (BED). All subjects ate two multicourse meals in the laboratory, and were given tape-recorded instructions at each meal either to binge or eat in a normal fashion. Subjects with BED consumed significantly more energy than did subjects without BED at both the binge [12,400 vs 8440 kJ (2963 vs 2017 kcal), P < 0.005] and normal [9810 vs 6870 kJ (2343 vs 1640 kcal), P < 0.02] meals. During the binge meal subjects with BED consumed a greater percentage of energy as fat (38.9% vs 33.5%, P < 0.002) and a lesser percentage as protein (11.4% vs 15.4%, P < 0.01) than did subjects without BED. There were no differences in macronutrient composition of food choices between groups in the normal meal. Obese women who meet criteria for BED show differences in both intake and macronutrient composition of food choices from obese women who do not meet these criteria when asked to eat in a laboratory setting, supporting the validity of this new diagnosis.

Almost anyone who has ever lost weight can attest that it is harder to sustain weight loss than to lose weight. Maintenance of a 10% or greater reduced body weight is accompanied by decreases in energy expenditure to levels significantly below what is predicted solely on the basis of weight and body composition changes. This disproportionate decline in energy expenditure would not be sufficient to account for the over 80% recidivism rate to pre-weight loss levels of body fatness after otherwise successful weight reduction if there were a corresponding reduction in energy intake. In fact, reduced body weight maintenance is accompanied by increased energy intake above that required to maintain reduced weight. The failure to reduce energy intake in response to decreased energy output reflects decreased satiation and perception of how much food is eaten and multiple changes in neuronal signaling in response to food which conspire with the decline in energy output to keep body energy stores (fat) above a CNS-defined minimum (threshold). Much of this biological opposition to sustained weight loss is mediated by the adipocyte-derived hormone "leptin".

Precise temporal relations between feeding and drinking were obtained by recording their occurrence simultaneously and continuously. The ingestion pattern of normal rats was comprised of discrete meals preceded or followed by drafts of water 78% of which ranged in size .5-2.5 ml. Drafts within the meal were rare and within the same size range. Desalivate neurologically normal rats and recovered lateral rats showed prandial drinking, a pattern in which all drinking occurred within the meal, in minute (<.5 ml.) drafts taken immediately after the ingestion of single 45-mg. food pellets. After desalivation a slow transition to the prandial drinking pattern occurred. These differences in patterns suggest that foodassociated drinking in the normal rat is controlled primarily by internal cues related to body-water need, while prandial drinking is learned in response to the necessity to swallow dry food from a dry mouth.