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.

stomach distension combine to reduce food intake in humans. Am J Physiol Regul Integr Comp Physiol 285: R992-R998, 2003. First published August 14, 2003 10.1152/ajpregu. 00272.2003.-The aim of this study was to test the hypothesis that gastric distension can enhance the effect of cholecystokinin (CCK) on reduction of food intake in men and women. Eight normal-weight subjects of each gender were tested four times each with either CCK or saline infusion crossed with gastric distension or no distension. Intravenous infusion of a low dose of CCK octapeptide (CCK-8; 112 ng/min for 23 min) combined with a subthreshold gastric distension induced by a water-filled balloon (300 ml) resulted in a significant (means Ϯ SED: 191 Ϯ 61 g in men, 209 Ϯ 61 g in women, and 200 Ϯ 43 g combined) reduction in intake of a liquid meal compared with saline infusion and unfilled gastric balloon. This combined effect was the result of a large and significant CCK effect when the stomach was distended (CCK vs. saline with distension: 169 Ϯ 43 g) and a small and insignificant distension effect (distension vs. no distension without CCK: 31 Ϯ 43 g). The CCK effect alone on intake (CCK vs. saline) without distension was not significant in men (72 Ϯ 61 g) but was significant in women (121 Ϯ 61 g). These results are consistent with the hypothesis that CCK's suppression of food intake is enhanced when the stomach is distended. satiety; feeding; gastric distension CHOLECYSTOKININ (CCK), a peptide hormone released by the duodenum mainly in the presence of digestion products of fats and proteins (5), reduces food intake in a variety of species, including humans (see Ref. 21 for a review). Physiologically, CCK stimulates pancreatic enzyme secretion (8), induces gall bladder contractions (1), increases neural activity in the gastric vagal afferents (18), relaxes the stomach, constricts the pylorus (13, 20), and inhibits gastric emptying when food is in the stomach (2, 12), thereby increasing gastric distension.It has been suggested that the increased gastric distension induced by slowing of gastric emptying may be the mechanism by which CCK reduces food intake (15). In support of this hypothesis, Moran and McHugh (15) reported that in monkeys a saline preload was necessary to decrease food intake after a low dose of CCK. In humans, Muurahainen et al. (17) demonstrated that intake of a test meal was significantly lower when CCK octapeptide (CCK-8) was given after a 500-g but not a 100-g soup preload. Without both CCK and the larger preload, no significant decrease in intake was observed. CCK infusion significantly decreased gastric emptying and thereby increased the gastric volume remaining after subjects ingested 500 g of soup. The size of the gastric volume increase after CCK was 80 g (from 230 to 310 g) after 25-30 min (end of ad libitum meal) compared with saline infusion (16). However, the reduction in gastric emptying also reduced the amount of nutrients entering the intestine. Therefore, the question was which of the stimuli provided by the ...

The animal model of exercise-induced anorexia was employed in humans to develop a laboratory paradigm for studying the acute effect of exercise on food intake. Each of nine obese and nine nonobese women exercised either strenuously (90 W) or moderately (30 W) on a cycle ergometer for 40 min or rested in the laboratory on each of 3 nonconsecutive days. Intake of a liquefied test meal (1.04 kcal/g) eaten 15 min after exercise was significantly less after the strenuous (620 g) than after the moderate (754 g) exercise in the nonobese women but was no different after the two conditions (532 g after strenuous, 581 g after moderate) in the obese women. Heart rate and energy expenditure were increased in proportion to the exercise by the same amount in both groups. The results demonstrate for the first time that food intake is reduced immediately after strenuous exercise in nonobese women, as it is in animals, and validate the feasibility of this laboratory paradigm.

Eating behavior of women with bulimia was compared with that of control subjects who had no eating disorders. Both groups were presented with two buffet-style multiple-item meals. In one meal subjects were instructed to eat normally and in the other they were instructed to eat as much as they could. The eating patterns of patients differed from control subjects in the quantity of food selected and in the rate of eating. During the binge meal, patients spent more of their meal time eating dessert and snacks than did control subjects and began their dessert and snack consumption earlier than control subjects. Patients distributed their meat consumption more evenly across the meal, whereas control subjects ate meat predominantly early in the meals. Most patients consumed either more or less than control subjects when not binge eating, indicating that the eating disturbances in bulimic patients are not confined to episodes of binge eating.

A universal eating monitor has been developed that permits covert continuous weighing of a subject's plate or other food reservoir by means of a concealed electronic balance. By coupling the device with a digital computer, it is possible to record precisely the amount consumed every 3 s throughout a single-course meal consisting of a relatively homogeneous mixture of foods. The monitor have been used to compare total intake, meal duration, initial rate of intake, and deceleration of intake in human subjects ingesting either a solid or liquid version of the same food after 3 or 6 h without food. It was found that the liquid form was eaten faster than the solid form, but that total amounts consumed in each form were not significantly different. These results suggest that when the rate of consumption is controlled by the physical consistency of the food, the amount eaten is not determined by the rate of consumption alone. Further studied are necessary to determine the relative roles of visual cues and interoceptive signals on quantity eaten.