Effects of caloric manipulations on food intake in baboons

Food intake of seven adult male baboons (Papio cynocephalus anubis) was monitored during daily 22-h experimental sessions. Food was available under a two-component operant schedule. Following completion of the first "procurement component" response requirement, access to food, i.e. a meal, became available under the second "consumption component," during which each response produced a 1-g food pellet. After a 10-min interval in which no response occurred, the consumption component was terminated. The effects of caloric preloads on food intake were determined by giving each baboon a meal of preferred foods 45-60 min prior to the start of the daily session. Caloric preloads decreased food intake during the first 8 h of the session, but had no effect on intake during the entire session. The effects of acute deprivation on food intake were determined by terminating sessions after a baboon had consumed 20-80% of baseline intake, and by starting a session 4-12 h late. Deprivation did not increase subsequent food intake. The effects of the availability of an alternative source of calories on total daily intake were determined by providing access to a dextrose solution. Baboons decreased intake of solid food in accordance with the caloric intake from the dextrose solutions by decreasing the number of meals. Finally, the effects of providing a diet of higher caloric density on food intake were determined. Two of the four baboons tested in this procedure maintained baseline levels of daily caloric intake, while the other two baboons increased daily caloric intake. In summary, free-feeding baboons were relatively insensitive to acute changes in feeding conditions, but were sensitive to long-term changes in the caloric content of available foods.     

Effect of operative stress on food intake and feeding pattern in female rats.

Effects of operative stress on food intake, meal size, and meal number were measured in 15 female rats before and after jugular vein catheterization. All rats had 5-d estrous cycles which correlated with cyclical feeding patterns that were most prominent during dark phase eating. In proestrous, meal number peaked (30.3+/-1.32), and meal size reached a nadir (0.33+/-0.02 g) with some corresponding change in food intake (9.8+/-0.38 g). Following operation on day 11, the cyclical variation of food intake, meal number, and meal size with estrous cycle was lost for the first 3 d, as was the diurnal rhythm in food intake. Eight rats recovered their dark phase feeding pattern by day 17 (recovered group), while 7 had not done so even by day 24 (non-recovered group). Food intake decreased to 40% of baseline in the recovered group and to 25% in the non-recovered group on day 11, increasing to 70% by day 14 in both groups and matching preoperative levels by day 17. Similar postoperative decreases were observed in meal number and meal size. Light phase feeding was increased, the ratio of day to night food intake being three times preoperative levels even at day 24. Preoperatively, non-recovered rats were similar to the recovered rats in all feeding indexes and continued to have estrous cycling in vaginal smears postoperatively. In the non-recovered rats, meal size more than doubled and meal number was depressed by 47% of preoperative levels and remained low until the end of the study. We conclude that operative stress disrupted cyclical and diurnal rhythms in food intake. In female rats, meal size is the first index to recover, increasing temporarily to maintain food intake.     

Cholecystokinin and satiety: current perspectives

In the almost 30 years since the ability of peripheral administration of the brain/gut peptide cholecystokinin (CCK) to inhibit food intake was first demonstrated, significant progress in our overall understanding of the role of CCK in ingestive behavior has been made. A physiologic role for endogenous CCK in the control of meal size has been demonstrated and sites and mechanisms of action for CCK in food intake have been investigated. Recent work has uncovered roles for the CCK satiety pathway in the mediation of the feeding modulatory actions of estradiol, insulin, and leptin. The availability of the Otsuka Long Evans Tokushima Fatty (OLETF) rat, a strain lacking CCK(A) receptors, provides a unique model for the study of how deficits in a within-meals satiety signaling pathway may result in long-term changes in food intake and body weight.     

Alternation between foods within a meal. Influence on satiation and consumption in humans

Food habituation/dishabituation has been observed in non-human primates in neurophysiological investigations of feeding, and in humans, through salivation or hedonic responses to food. The objective of the study was to evaluate in humans the effect of disruption of habituation by alternation between foods in a meal. Sixteen volunteers (8 males, 8 females; age: 21 ± 1 yr; BMI: 21.5 ± 0.5 kg m⁻²) ate a two-course meal [meatballs (M) and fries (F), then vanilla cream (C) and brownies (B)] during three randomized sessions. Sessions differed by the alternation of these foods: No-Repetition session with M-F–C-B; Single-Repetition session with F-M-F–B-C-B; Multiple-Repetition session with M-F-M-F-M-F–C-B-C-B-C-B. Final intakes of F and B were ad libitum. Quantities consumed (g, kJ) and ratings of hunger, pleasantness and desire to eat each food were evaluated. Compared to the No-Repetition session, subjects ate 18% more fries and 16% more brownies in the Single-Repetition, and 13% more fries but 20% less brownies in the Multiple-Repetition session. Pleasantness for the food decreased from before to after intake for both fries and brownies with no significant difference between the sessions. It therefore appears that moderate alternation between foods at lunch increases intake, but multiple alternations of foods at the end of the meal may decrease consumption. These differences in intakes could result from differences in sensory-specific satiety via disruption of habituation.     

Hypothalamic dopamine and serotonin in the regulation of food intake

Because daily food intake is the product of the size of a meal and the frequency of meals ingested, the characteristic of meal size to meal number during a 24-h light-dark cycle constitutes an identifiable pattern specific to normal states and obesity and that occurs during early cancer anorexia. An understanding of simultaneous changes in meal size and meal number (constituting a change in feeding patterns) as opposed to an understanding of only food intake provides a more insightful dynamic picture reflecting integrated behavior. We have correlated this to simultaneous changes in dopamine and serotonin concentrations and to their postsynaptic receptors, focusing simultaneously on two discrete hypothalamic food-intake-related nuclei, in response to the ingestion of food. The relation between concentrations of dopamine and serotonin limited to the lateral hypothalamic area (LHA) and the ventromedial nucleus (VMN) as they relate to the influence of meal size and meal number during the hyperphagia of obesity and anorexia of cancer as measured in our experiments are discussed. Based on these data, conceptual models are proposed concerning: 1) an "afferent-efferent neurotransmitter unit," with facilitatory or inhibitory neuropeptide properties to generate an appropriate neuroendocrine and neuronal response that ultimately modifies food intake; 2) initiation and termination of a meal, thereby determining the number and size of a meal under normal conditions; and 3) a schema integrating the onset mechanism of cancer anorexia. Nicotine is used as a tool to further explore the relation of meal size to meal number, with a focus on simultaneous changes in dopamine and serotonin concentrations in the LHA and VMN with the onset of acute anorexia of nicotine infusion and acute hyperphagia of nicotine cessation. Data concerning the role of sex-related hormones on dopamine and serotonin with regard to the LHA and VMN in relation to the modulation of food intake are also presented.     

Meal-timing, circadian rhythms and life span of mice

The possibility that circadian rhythm alteration may contribute to the life-prolonging effect of food restriction was investigated in female CD2F1 mice housed in a room with a 12-h span of fluorescent lighting daily. A control group was allowed to feed ad libitum throughout life while three other groups began lifelong restriction to about 75% of ad libitum intake when 6 wk old. The daily schedule of food accessibility differed among these three groups: a single meal during early darkness; a single meal during early light; six smaller meals at about 2-h intervals during darkness. Food restriction as such clearly prolonged life, but there were no statistically significant differences in overall mean life span or in 10th-decile life span among the three restricted groups. Telemetered body temperature data confirmed marked differences in the effects of these different restricted feeding schedules on circadian rhythms. The effect of food restriction on survival is probably not due to altered relations among circadian rhythmic variables. Possible contributing factors suggested by the results are a lower body temperature, a reduced overall metabolic rate and an increased circadian amplitude.     

Effect of adrenergic blockers and depleters on food intake in rats

In rats kept at a constant temperature (24 +/- 1.5 degrees C) and on a reversed day/night cycle (light from 11 p.m. to 11 a.m.), the amount of food eaten during the first 2 h of darkness and during 24 h was measured every day. When reserpine or guanethidine were injected 5 min before the beginning of the dark period on four consecutive days, there was no significant change in the 0.5-, 1-, or 24-h food intake on the injection days, but there was a significant increase in the 0.5-, 1- and 2-h food intake during the next five to eight days, without any change in the 24-h intake. A single injection of dichloroisoproterenol produced no change on the day of injection but it induced a significant increase in the 0.5-, 1- and 2-h intake on the following 15 days, without any change in the 24-h intake. The increase in the early night-time feeding without any change in the 24-h intake was interpreted as an increase in meal size (diminished preabsorptive satiation) compensated by a decrease in meal frequency. Both reserpine and guanethidine are catecholamine depleters but the latter does not penetrate into the brain. Dichloroisoproterenol is a beta-blocker acting on the glycogenolytic effects of catecholamines. The results thus agree with the hypothesis that glycogenolysis elicited by the liberation of intrahepatic catecholamines from the sympathetic nerve endings and chromaffin cells plays a role in preabsorptive satiation.     

Differential feeding patterns induced by tumor growth and by TPN.

The effects of anorexia induced by early tumor, and anorexia induced by total parenteral nutrition (TPN) on food intake and the indexes of food intake, were investigated in rats infused with saline after jugular catheter placement and concomitant inoculation with methylcholanthrene (MCA)-induced tumor cells on day 0, and in rats without catheters receiving tumor only. Tumor became palpable around day 10 and increased to represent 6-8% of host body weight by day 26. On day 18, food intake started to decrease. Catheter-bearing rats were then randomized to saline controls (n = 9) for 11 d or to TPN-100 (n = 9) for 4 d providing 100% of daily caloric needs. Both then received saline until day 26. Food intake and feeding indexes were continuously measured using the Automated Computerized Rat Eater Meter (ACREM) and data was analyzed using ANOVA and regression analysis. In controls (both with and without catheter) the tumor induced a specific feeding pattern which consisted of a significant (P < 0.01) decrease in food intake via a significant (P < 0.05) decrease in meal size. A non-significant decrease in meal number and meal duration occurred. Two other feeding-related activities, meal consumption rate and intermeal sniffs, also decreased. Infusion of TPN-100 into the already anorectic rat led to a further significant (P < 0.0001) decrease in food intake via a significant decrease in both meal size (P < 0.0001) and in meal number (P < 0.0001). A decrease in all other feeding indexes also occurred, resulting in a different feeding pattern. After stopping TPN-100, the TPN-100-induced feeding pattern returned to that of the tumor-induced feeding pattern. That the tumor-induced feeding pattern differs from the TPN-100-induced feeding pattern suggests that the mechanisms whereby these two factors induce anorexia may also differ.     

Interaction of fat availability and sex on postprandial satiety and cholecystokinin after mixed-food meals

BACKGROUND: Cholecystokinin (CCK) is associated with fat-induced satiety. OBJECTIVE: The primary objective of the present study was to determine, in an acute meal setting, whether the availability of dietary fat for alimentary processing, and hence the stimulation of CCK, affects the postmeal satiety response in men and women. DESIGN: In a within-subjects design, subjects (8 men, 7 women) consumed 1 of 3 isoenergetic mixed-food test meals 1 wk apart in random order. The test meals contained 30% of energy from fat, of which more than two-thirds was derived from whole almonds, almond oil, or a mix of safflower and corn oils. Visual analogue scales were used to assess indexes of satiety at defined time points up to 6 h after meal consumption. Blood was sampled at corresponding time points for measurement of CCK, glucose, insulin, and triacylglycerol. Subsequent food intake was also assessed. RESULTS: All meals suppressed hunger and induced a pattern of satiety that was sex-specific and corresponded with the CCK response. Women had higher plasma CCK concentrations and experienced greater satiety after the almond oil and control meals (fat as oil) than after the whole almond meal (fat in whole food structure). Men showed no differential response among meals for CCK and satiety. Plasma triacylglycerol differed by time among meals but not by sex, and no significant differences in glucose and insulin were found. CONCLUSIONS: The satiety response to dietary fat provided in oil or whole food form is influenced by sex and is dependent on the availability of fat to stimulate CCK release in women but not in men.     

Adherence to Diet and Meal Timing in a Randomized Controlled Feeding Study of Time-Restricted Feeding

Adherence is critical in feeding studies to determine the efficacy of dietary interventions. This time-restricted intake of meals (TRIM) investigation was a controlled feeding study that randomized 41 participants to follow 12 weeks of time-restricted feeding (TRF) or a usual feeding pattern (UFP). Adherence was optimized through careful screening and participant orientation, flexibility in beverages and seasonings, and frequent contact between participants and staff. Adherence was measured daily using a self-administered diary form. We calculated the percentage of participant-days with perfect adherence to meal timing (ate all meals within their designated time window) and to food consumption (ate all study food and no non-study food). Adherence was compared between study arms, days of the week, and weeks of the study period using generalized estimating equations (GEE) regression. There was perfect adherence to meal timing on 87% of participant-days and to food consumption on 94% of participant-days, with no significant difference by arm. In UFP, but not TRF, participants had lower adherence to meal timing over the weekend (p-value = 0.002) and during the first two weeks of intervention (p-value = 0.03). A controlled feeding study randomizing free-living individuals to different meal timings achieved a high degree of adherence to meal timing and food consumption, utilizing multiple strategies.     

Assessment of dietary intake among Moroccan women and Surinam men

Objective. To establish a method for food consumption data collection in ethnic groups in the Netherlands. Methods. Two pilot studies have been carried out, one among Moroccan women and one among Surinam men. First, focus group discussions were held to obtain background information from members of the target population. For food consumption assessment 2 2 24-h recall was chosen. Furthermore, background information on age, place of birth, frequency of visits to Morocco or Surinam, Dutch language skills, meal pattern, food purchases and antropometric measurements were taken. Results. It was found that the diets of both Moroccan women and Surinam men tended to approach the recommended daily intake of macronutrients more than the average intake of a Dutch person. However, reported energy and micronutrient intake on the second day of the dietary recall was lower than on the first recall day. Conclusion. The 24-h recall is a suitable method for food consumption measurements among Moroccan and Surinam people. On the other hand, the interviewer must be aware of potential under-reporting, especially during the second recall.     

Satiety and test meal intake among women with binge eating disorder

OBJECTIVE: The purpose of the study was to measure test meal consumption and the changes in hunger and fullness during a test meal in obese individuals with and without binge eating disorder (BED) and normal-weight controls. METHOD: Twelve women with BED, 12 obese control participants, and 12 normal-weight control participants participated in two single-item test meal sessions. In one session participants were instructed to "binge," and the other eat a normal meal. Participants made ratings of hunger and fullness on visual analog scales after every 75-g increment of food. RESULTS: In comparison to obese or normal-weight controls, patients with BED consumed significantly more food to reach a similar level of fullness or hunger. CONCLUSION: Individuals with BED consumed significantly more food and showed blunted changes in hunger and fullness during both the binge and nonbinge meals. These findings suggest that individuals with BED may have disturbances in satiety that in some ways resemble those described among individuals with bulimia nervosa.     

Rapid fall in plasma threonine followed by increased intermeal interval in response to first ingestion of a threonine-devoid diet in rats

In most animals, ingestion of a diet lacking an essential amino acid (EAA) gives rise to anorexia within a few hours. The first signal in this feeding response may be the fall in plasma levels of the limiting EAA. In the present study, we measured plasma amino acid levels and food intake after the first exposure to either a threonine-devoid (THR-DEV) or corrected (COR) diet in 16 rats bearing a chronic jugular catheter for blood sampling. Food intake was reduced 165 min (p<0.05) after presentation of the THR-DEV diet. Analysis of the feeding pattern showed that intake was reduced via a four-fold lengthening of the second inter-meal interval. Plasma threonine levels started to fall between 30 and 60 min after onset of the meal (p<0.05). These results, observed in the same rats, lend further support for an early modification of the plasma amino acid pattern in relation to the decrease in feeding of a diet that is EAA deficient.     

Learned food-cue stimulates persistent feeding in sated rats

Cues that predict food can stimulate appetite and feeding independent of physiological hunger. How long such effects might last is currently unknown. Here we began to characterize long-term effects in a rodent model of cue-potentiated feeding. Rats were conditioned to associate a tone with food pellets distinct from their regular laboratory chow, and then were tested along with controls for food consumption following tone presentations. In Experiment 1, rats were tested under sated or food-deprived conditions to determine whether fasting would augment cue-driven feeding. Rats in the control group regulated intake based on physiological state, while conditioned rats consumed similar large amounts of food regardless. Experiment 2 tested the durability of cue-potentiated feeding to repeated testing in sated rats. We observed robust cue-potentiated feeding during the first two tests, while in the third and fourth tests both groups ate similar large amounts of pellets. In both experiments the conditioned tone-cue induced binge-like consumption of the cued food and persistent feeding for the duration of 4-h tests. Rats then failed to adjust daily chow consumption to account for their increased intake post-cue. In summary, brief cue priming stimulated substantial intake in sated states that was behaviorally uncompensated for by homeostatic mechanisms.     

VMN/LHA functional inhibition in tumor-bearing rats suggests hypothalamic involvement in cancer anorexia

Food intake is mainly controlled in the hypothalamus via a series of functionally related nuclei, including the ventromedial nucleus of hypothalamus (VMN) and the lateral hypothalamic area (LHA). Since food intake is the product of meal number and meal size, we investigated the role of the VMN and LHA in influencing these feeding indices and in mediating cancer anorexia in tumor-bearing (TB) rats, via temporarily inhibiting VMN or LHA. Adult male Fischer-344 rats (n = 23) inoculated with 106 MCA sarcoma cells were studied. When anorexia developed, rats were randomly assigned to stereotaxically located bilateral intra-VMN or intra-LHA microinjections of the neuronal blocker colchicine (CX; n = 6 each group) or saline (n = 6 and n = 5, respectively). Non TB rats (NTB; n = 7) served as controls. Food intake and feeding indices were recorded by a computerized device. At onset of anorexia, a reduction of meal number occurred, leading to reduced food intake. After inhibition of VMN activity by CX, meal number significantly increased, so that food intake increased and almost normalized. In contrast, intra-LHA microinjection of either CX or saline resulted in reduction of meal size, leading to reduced food intake and death. Findings suggest that VMN and LHA influence meal number and meal size, respectively. Since cancer anorexia mainly results from an initial reduction of meal number and the inhibition of VMN led to an increase in meal number, the early effect of tumor growth on VMN activity may be an early step leading to reduced food intake.     

Afferent signals regulating food intake

Food intake is a regulated system. Afferent signals provide information to the central nervous system, which is the centre for the control of satiety or food seeking. Such signals can begin even before food is ingested through visual, auditory and olfactory stimuli. One of the recent interesting findings is the demonstration that there are selective fatty acid taste receptors on the tongue of rodents. The suppression of food intake by essential fatty acids infused into the stomach and the suppression of electrical signals in taste buds reflect activation of a K rectifier channel (K 1.5). In animals that become fat eating a high-fat diet the suppression of this current by linoleic acid is less than that in animals that are resistant to obesity induced by dietary fat. Inhibition of fatty acid oxidation with either mercaptoacetate (which blocks acetyl-CoA dehydrogenase) or methylpalmoxirate will increase food intake. When animals have a choice of food, mercaptoacetate stimulates the intake of protein and carbohydrate, but not fat. Afferent gut signals also signal satiety. The first of these gut signals to be identified was cholecystokinin (CCK). When CCK acts on CCK-A receptors in the gastrointestinal tract, food intake is suppressed. These signals are transmitted by the vagus nerve to the nucleus tractus solitarius and thence to higher centres including the lateral parabrachial nucleus, amygdala, and other sites. Rats that lack the CCK-A receptor become obese, but transgenic mice lacking CCK-A receptors do not become obese. CCK inhibits food intake in human subjects. Enterostatin, the pentapeptide produced when pancreatic colipase is cleaved in the gut, has been shown to reduce food intake. This peptide differs in its action from CCK by selectively reducing fat intake. Enterostatin reduces hunger ratings in human subjects. Bombesin and its human analogue, gastrin inhibitory peptide (also gastrin-insulin peptide), reduce food intake in obese and lean subjects. Animals lacking bombesin-3 receptor become obese, suggesting that this peptide may also be important. Circulating glucose concentrations show a dip before the onset of most meals in human subjects and rodents. When the glucose dip is prevented, the next meal is delayed. The dip in glucose is preceded by a rise in insulin, and stimulating insulin release will decrease circulating glucose and lead to food intake. Pyruvate and lactate inhibit food intake differently in animals that become obese compared with lean animals. Leptin released from fat cells is an important peripheral signal from fat stores which modulates food intake. Leptin deficiency or leptin receptor defects produce massive obesity. This peptide signals a variety of central mechanisms by acting on receptors in the arcuate nucleus and hypothalamus. Pancreatic hormones including glucagon, amylin and pancreatic polypeptide reduce food intake. Four pituitary peptides also modify food intake. Vasopressin decreases feeding. In contrast, injections of desacetyl melanocyte-stimulating hormone, growth hormone and prolactin are associated with increased food intake. Finally, there are a group of miscellaneous peptides that modulate feeding. beta-Casomorphin, a heptapeptide produced during the hydrolysis of casein, stimulates food intake in experimental animals. In contrast, the other peptides in this group, including calcitonin, apolipoprotein A-IV, the cyclized form of histidyl-proline, several cytokines and thyrotropin-releasing hormone, all decrease food intake. Many of these peptides act on gastrointestinal or hepatic receptors that relay messages to the brain via the afferent vagus nerve. As a group they provide a number of leads for potential drug development.     

Cigarette smoking and the thermic responses to isocaloric meals of varying composition and palatability

The 4-h thermic responses to glucose and a liquid formula meal (Study 1), and to a solid food 'breakfast' meal and the liquid formula meal (Study 2) were measured in a group of young weight-stable female subjects. The groups recruited for the two studies consisted of nine smokers and seven non-smokers (Study 1) and six smokers and eight non-smokers (Study 2). The habitual smokers presented after a 12-h abstention from cigarettes but were permitted to smoke following the meal; their thermic responses were thus due to the combined thermogenic effects of smoking and feeding. The mean thermic responses to all three types of meal were greater for the smokers than for the non-smokers, and the magnitude of this difference was similar irrespective of the type of meal given (range 52 kJ-70 kJ). The thermic responses to the liquid formula meal tended to be greater than those to an isocaloric glucose load for smokers and non-smokers (Study 1). In Study 2, the increase in energy expenditure occurring during the first hour following the 'breakfast' meal was consistently greater than the 1-h response to the liquid formula meal. The larger thermic response to feeding to all three meal-types observed in the groups of smokers when compared with non-smokers, is attributed to the actions of cigarettes smoked (mean 4.6) during the period of measurement. It is concluded that whilst the thermic response to feeding is augmented in cigarette smokers this increase is an additive effect and is independent of the size and nature of the thermic effect of the meal.     

An interaction between hypothalamic glucagon-like peptide-1 and macronutrient composition determines food intake in rats

Glucagon-like peptide-1 (GLP-1) release in response to food ingestion has been associated with decreased food intake. In the present study, we tested the hypothesis that the feeding response to GLP-1 injection into the hypothalamic paraventricular nucleus (PVN) is influenced by the macronutrient composition of the food consumed. In the first experiment, rats were injected with GLP-1 (0.2 microg) or saline (0.5 microL) in the PVN at dark onset (1800 h), and food intake from a maintenance diet (18% protein) was measured at 1, 2 and 14 h. In Experiment 2, after GLP-1 injection, rats were fed a carbohydrate (protein-free) diet for the first 2 h or gavaged with glucose (1.4 g/5 mL). In Experiment 3, after GLP-1 injection, rats were fed a protein (50%) diet for the first 2 h, or were preloaded with egg albumin (1.0 g). In the last experiment, GLP-1 was given after corn oil gavage (2.4 g). GLP-1 injection resulted in a reduced consumption of the maintenance diet from 2 to 14 h. The decreased food intake from 2 to 14 h after GLP-1 administration occurred after carbohydrate intake, either by meal or preloads, but not after protein intake, either as a meal or preload. A transient interaction of GLP-1 with a corn oil gavage was detected but only in early feeding (0-2 h). We conclude that the effect of GLP-1 injected in the PVN on food intake is influenced by the macronutrient composition of the food consumed. Carbohydrate enhances, protein blocks and corn oil has a transient effect on the suppression of food intake caused by GLP-1 in the PVN.     

Effects of short-chain fructooligosaccharides on satiety responses in healthy men and women

In view of a dramatic increase in the incidence of obesity, the present study examined the appetite effects of a functional fiber as a potential dietary intervention. Fiber may increase satiety. Satiety effects also may be linked to colonic fermentation. Short-chain fructooligosaccharide (scFOS) are fermentable fibers that can be added to foods to influence these actions. The primary objective of this study was to determine if scFOS affects satiety and hunger and has an additive effect on food intake. Using a double-blind crossover design, 20 healthy subjects were assigned to consume two separate doses of 0 g, 5 g, or 8 g of scFOS. The first dose was mixed into a hot cocoa beverage and served with a breakfast meal of a bagel and cream cheese. A beverage was used in the test meal due to the ease with which scFOS can be added to this medium. Satiety was assessed with visual analogue scales (VASs) at 0, 15, 30, 45, 60, 90, 120, 180, and 240 min. Ad libitum food intake was measured at a lunch meal provided at the test site at 240 min. Subjects then recorded their food intake over the remainder of the 24-h study day. The second dose of scFOS was consumed in the form of 3 solid, chocolate-flavored chews (51-67 total kcal) without additional food or drink, 2h prior to the subject's dinner meal. Breath hydrogen measures were collected prior to the breakfast test meal (0 min) and the ad libitum lunch (240 min). Gastrointestinal tolerance was evaluated over the course of the 24-h study day using VAS. All treatments were well tolerated. No differences in subjective satiety over the morning, or food intake at lunch, were found. Over the remainder of the day, the high dose of scFOS reduced food intake in women, but increased food intake in men, suggesting a gender difference in the longer-term response. Breath hydrogen, used as a marker of fermentation, increased in a dose-dependent manner. These results indicate that scFOS undergoes fermentation within 240 min; however, acceptable amounts of scFOS did not enhance acute satiety or hunger.     

Effects of dietary and pharmacological manipulations on appetitive and consummatory aspects of feeding in non-human primates

This study examined how pharmacological and behavioral manipulations affect appetitive and consummatory aspects of feeding of baboons. Baboons have access to food 24 h each day, but they must complete a two-phase operant procedure in order to eat. Responding on one lever during a 30-min appetitive phase was required before animals could start a consumption phase, i.e. a meal, where responding on another lever led to food delivery. Responding during the appetitive phase resulted in presentations of food-related stimuli only. Decreasing session length, increased appetitive behavior and increased meal size. Limiting the number of meals to a single 90 min meal each day but increasing the number of food pellets the animals received increased the size of meal, but did not increase appetitive behavior. These findings suggest that time since the previous meal has a greater effect on appetitive behavior than the size of the previous meal. Amphetamine (AMPH), which increases dopamine, decreased food intake at doses that did not affect appetitive behavior, indicating that appetitive and consummatory aspects of eating can be pharmacologically differentiated. Increasing how frequently animals could earn food-related stimuli in the appetitive phase and food in the consummatory phase increased both appetitive and consumatory behavior. Under these conditions, AMPH nearly doubled appetitive behavior at doses that decreased food intake by nearly 50 percent. When animals had one meal, of self-determined duration, meal size increased without affecting appetitive behavior, further demonstrating that appetitive behavior can be independent of the size of the previous meal and not predictive of the size of the subsequent meal. Under these conditions, AMPH decreased food intake at doses that did not affect appetitive behavior. In contrast, dexfenfluramine (DFEN), which increases serotonin, decreased both appetitive and consumatory behavior. Thus, it is possible to independently manipulate the appetitive and consummatory aspects of eating using both pharmacological and behavioral interventions indicating that it may be possible to develop medications that selectively affect appetitive or consummatory aspects of eating.