Spontaneous Meal Research Articles

Social facilitation of food intake is mediated by meal duration

The effect of the number of others present on the amount of food eaten was investigated in the Netherlands by studying spontaneous meal size in 50 free-living young males and females. Subjects recorded food consumption, number of others present, hunger, taste of the food, food availability, and atmosphere at each eating or drinking moment for four ( n = 30) or seven consecutive days ( n = 20). The results of the study with four and the study with seven recording days were comparable. The mean Pearson within-person correlation coefficient between the number of others present and meal size was 0.24 ( n = 50, p < 0.05). This correlation was significant for breakfast (0.40, p < 0.05) and snacks (0.18, p < 0.05), but not for lunch ( r = 0.19, p > 0.05) and dinner ( r = 0.15, p >; 0.05). A path analysis showed no direct effect of the number of others on meal size, but revealed that social facilitation of spontaneous meal size was mediated by meal duration.

Spontaneous meal size is increased by hepatic portal infusion of insulin antibodies, but unaffected by insulin infusion: W. Langhans, D. Surina and N. Geary.* Institute for Animal Sciences, Swiss Federal Institute of Technology, 8092 Zurich, Switzerland, and * Bourne Laboratory, New York Hospital-Cornell Medical Center, White Plains, NY 10605, U.S.A.

Spontaneous meal size is increased by hepatic portal infusion of insulin antibodies, but unaffected by insulin infusion: W. Langhans, D. Surina and N. Geary.* Institute for Animal Sciences, Swiss Federal Institute of Technology, 8092 Zurich, Switzerland, and * Bourne Laboratory, New York Hospital-Cornell Medical Center, White Plains, NY 10605, U.S.A.

Push-pull perfusion reveals meal-dependent changes in the release of bombesin-like peptides in the rat paraventricular nucleus

Bombesin (BN)-like peptides have been implicated in the regulation of ingestive behavior. The main objective of the present study was to monitor the dynamics of central BN-like peptide release in relationship to spontaneous meal ingestion and termination. Peptide level fluctuations were determined using in vivo push-pull perfusion of the hypothalamic paraventricular nucleus (PVN) and off PVN sites, combined with ex vivo radioimmunoassay. Analysis across all meals revealed significant differences between preprandial, prandial and postprandial extracellular BN-like immunoreactivity (BLI) at the anterior aspect of the PVN, with about a 3-fold diminution during a meal as compared to before or after a meal. Meal-related fluctuations were not detected at more distal hypothalamic sites or at sites within the caudate nucleus. When the analysis was restricted exclusively to the first meal after dark onset, a similar pattern of change in the interstitial levels of PVN BLI was generally observed; levels being higher preprandially as compared to the prandially (albeit by a smaller magnitude), and the termination of the first meal being accompanied by a robust (about 3-fold) increase in BLI. This is the first demonstration of site specific in vivo release of BN-like peptides in relation to feeding status and it further supports the physiological role of this family of peptides in the regulation of food intake.

Insulin is a prandial satiety hormone

The present study assessed meal-contingent insulin effects on spontaneous meal patterns. Rats, trained to lever press for daily food requirements, showed stable meal patterns and were then implanted with hepatic-portal catheters. Once again stable in ingestion, animals received either physiological saline or vehicle plus 1 or 2 mU of regular, short-acting insulin beginning at 10 pellets into each initiated meal (which was the chosen minimum meal size definition). All meals during that day were then infused with the same solution and comparisons were made within animals (across days) only. Insulin reduced the size of spontaneous meals at both 1 mU ( p < .01) and 2 mU doses ( p < .001). No other meal parameters were significantly affected. In a complementary study, rats trained to lever press showed increases in meal size when “recovering from” a diazeoxide-adulterated diet (diazeoxide has been shown to limit insulin release). Thus, when insulin is increased during spontaneously taken meals, those meals are reduced in size and drugs which block insulin release, increase the size of meals; we assert insulin is a prandial satiety hormone which likely reduced feeding by increasing glucose uptake into peripheral tissue.

Lithium chloride and inescapable, unsignaled tail shock differentially affect meal patterns of rats

Several motivational states, such as malaise, fear, and satiety, reduce spontaneous food ingestion by rats, and differentiation of these states is often desirable. The present study used the spontaneous meal pattern to this end. The illness-inducing toxin lithium chloride delayed initiation of the first postinjection meal, and that meal was smaller and eaten more slowly (Experiments 1A and 1B). Rats exposed to tail shock also subsequently took longer to initiate meals, but meals were eaten faster and were slightly larger relative to control conditions (Experiment 2). These changes in meal patterns are different from those produced by satiely-related hormones, such as CCK or insulin, which solely reduce meal size in paradigms designed to assess physiological regulation of food intake. Taken together, these findings attest to the ability of meal patterns to distinguish malaise, fear, and satiety from one another.

The caloric demand of lactation does not alter spontaneous meal patterns, nutrient intakes, or moods of women

The regulation of food and fluid intake in lactating women was examined by comparing maternal intake during lactation, 6 weeks postpartum, to intake in two groups of nonpregnant, nonlactating women. All subjects completed a questionnaire and then filled out a food-intake diary for seven consecutive days. Lactating women did not differ from body weight-matched, nonlactating controls in their total daily intakes or their meal patterns. However, they consumed a significantly smaller percentage of the recommended dietary allowances (RDA) per day than did their nonlactating counterparts. Lactating women were also significantly more calm both pre- and postmeal than were either of the control groups. These results indicate that the lactating women, at 6 weeks postpartum, did not increase their intake to compensate for the caloric demands of lactation. This may indicate that the lactating women catabolize weight gained during pregnancy faster than accounted for in the RDA, or that lactating women increase their metabolic efficiency.

Glucagon acts in the liver to control spontaneous meal size in rats

To determine the site of origin of pancreatic glucagon's inhibitory effect on spontaneous feeding in rats, glucagon was infused into either the hepatic portal vein or the inferior vena cava during spontaneous meals late in the dark phase. Hepatic portal infusion of 1.7-13.6 micrograms glucagon/meal reduced spontaneous meal size. In contrast, these doses did not significantly affect meal size when delivered via vena caval catheters that ended near the junction of the hepatic vein. This difference indicates that glucagon receptor sites in the liver initiate the satiating action of glucagon during spontaneous meals. The vagal dependency of glucagon satiety was also tested. Hepatic portal infusion of 13.6 micrograms glucagon/meal reduced the size of spontaneous meals both early and late in the dark in neurally intact rats, but not in hepatic-vagotomized rats. Finally, antagonism of endogenous glucagon with hepatic portal infusion of glucagon antibodies in a dose sufficient to neutralize 1 ng glucagon in vitro increased spontaneous meal size in intact rats, but not in hepatic-vagotomized rats. Thus the satiating effects of both exogenous and endogenous glucagon on spontaneous food intake appear to depend on the hepatic branch of the vagus. Taken together, these results are consistent with the hypothesis that glucagon acts in the liver to produce a satiety signal that is transmitted to the brain by the hepatic branch of the abdominal vagus.

Patterns of duodenal osmolality in young pigs fed solid food

Duodenal hypertonicity can induce satiety, but whether duodenal osmolality varies during eating enough to influence meal size is not clear. To find out more about this, duodenal samples were taken via implanted catheters from 10 young pigs under three feeding conditions. 1) The pigs were fasted 4-5 h and then given a meal with drinking water available. Duodenal osmolality rose from a premeal level of 297 mosmol/kgH2O to a peak of 430 mosmol/kgH2O at 35 min after the meal began and then returned to the premeal level after 2.2 h. 2) When pigs were similarly fasted and then given a meal, but with no drinking water available during and after the meal, osmolality rose to 418 mosmol/kgH2O after 35 min and only returned to premeal levels after 4.2 h. 3) Finally, when pigs were allowed to eat and drink spontaneously, osmolality rose from a mean of 281 to only 308 mosmol/kgH2O after meals, in part because of water drinking in association with meals and in part because the spontaneous meals were smaller. The results demonstrate that duodenal osmolality can rise significantly after meals but that hyperosmolality is moderated by water drinking.

Hepatic portal infusion of glucagon antibodies increases spontaneous meal size in rats

Specific antibodies to pancreatic glucagon in a dose sufficient to neutralize 1.5 ng glucagon in vitro were intraportally infused during the first 2 min of spontaneous meals in ad libitum-fed male Sprague-Dawley rats. In separate tests, glucagon antibodies stimulated feeding during the first spontaneous meal of the dark phase (73% mean increase in meal size) and during spontaneous meals in the last quarter of the dark phase (58% increase). These results indicate that a glucagon-sensitive satiety mechanism has a physiological role in the control of nocturnal feeding in rats.

Hepatic portal glucagon infusion decreases spontaneous meal size in rats

We describe the first tests of intraportal pancreatic glucagon infusions during spontaneous meals in undisturbed, ad libitum-fed male Sprague-Dawley rats. Two-minute infusions beginning at meal onset and delivering 14 micrograms glucagon reduced the size and duration of both early and late nocturnal meals. After glucagon infusion during early nocturnal meals, neither the latency nor the size of the next meal was affected. Meal onset infusion of 3.4-14 micrograms glucagon/meal dose-dependently reduced late nocturnal meal size 19-64%. Full-meal glucagon infusions did not inhibit feeding more than 2-min infusions begun at meal onset or meal middle, despite fivefold differences in amount infused. These data indicate that spontaneous feeding is pharmacologically inhibited by prandial changes in hepatic portal glucagon concentration.

Social facilitation of the spontaneous meal size of humans occurs on both weekdays and weekends

The amount eaten by humans in spontaneously ingested meals is positively correlated with the number of other people present. This could be due to a social facilitation or may occur as an artifact of a covariation produced by changes in intake occurring over weekends. This possibility was investigated by paying 315 adult humans to maintain 7-day diaries of everything they ingested, when and where they ingested it, and the number of other people present. During weekends, larger meals were ingested, in the presence of more people than during weekdays. However, strong, positive, and significant correlations between meal size and the number of other people present were found separately for meals eaten only during weekdays and for those eaten only during weekends. The results suggest that the correlation results from a true social facilitation of eating and that this facilitation is an important determinant of the eating behavior of normal humans.

Social facilitation of the spontaneous meal size of humans occurs regardless of time, place, alcohol or snacks

The amount eaten by humans in spontaneously ingested meals is positively correlated with the number of other people present. This could be due to a social facilitation or may be produced as an artifact of a covariation produced by a third factor. Possible covariations produced by time and location of eating, alcohol intake, and snack/meal ingestion were investigated by paying 78 adult humans to maintain 7-day diaries of everything they ingested, when and where they ingested it, and the number of other people present. The results demonstrate that, although the covariances exist, they could not account for the social correlation. Strong, positive and significant correlations between meal size and the number of other people present were found separately for meals eaten during the breakfast period, the lunch period and the dinner period, eaten in restaurants, at home and elsewhere, eaten accompanied by alcohol intake or without alcohol, and for only snacks or only meals. The results suggest that the correlation results from a true social facilitation of eating and that this facilitation is an important determinant of eating regardless of whether alcohol is ingested with the meal, a snack or a meal is eaten and regardless of when or where it is eaten.

Pancreatic glucagon signals postprandial satiety

The hypothesis that prandial increases in circulating pancreatic glucagon initiates an important peripheral satiety signal is reviewed. Glucagon administration at the beginning of meals reduces the size of test meals in animals and humans and reduces the size of spontaneous meals in rats. Exogenous glucagon may also interact synergistically with cholecystokinin to inhibit feeding. These appear to be satiety effects because they are behaviorally specific in rats and subjectively specific in humans. Glucagon's pharmacological satiety effect is complemented by compelling evidence for a necessary contribution of endogenous glucagon to the control of meal size: administration of glucagon antibodies increases both test and spontaneous meal size in rats. Under many, but not all, conditions exogenous glucagon's satiety effect appears to originate in the liver and to be relayed to the brain via hepatic vagal afferents. Analysis of the central processing of this signal, however, has barely begun. How glucagon changes are transduced into neural afferent signals also remains an open question. The only hypothesis that has been extensively tested is that stimulation of hepatic glucose production initiates the satiety signal, but this is neither convincingly supported nor clearly rejected by currently available data. It is also not yet clear whether glucagon contributes to some forms of obesity or has potential use as a therapeutic tool in the control of eating disorders. Of the several proposed controls of hunger and satiety, glucagon appears to be one of the most likely to be physiologically relevant. This encourages further analysis of its behavioral characteristics, its neural mechanisms, and its clinical potential.

Social facilitation of duration and size but not rate of the spontaneous meal intake of humans

The amount eaten by humans in spontaneously ingested meals is positively correlated with the number of other people present. In order to investigate whether this social facilitation of eating was due to an increase in arousal, emotionality, hunger, or social interactions, analyses were performed on the data obtained from 82 adult humans. They were paid to maintain 7-day diaries of everything they ingested, when and where they ingested it, the number of other people present, and their subjective states of hunger, elation, and anxiety. The presence of other people was found to be associated with the duration of meals and not the rate of intake, whereas self-rated hunger was found to be associated with the rate of intake and not the duration of meals. Self-rated anxiety was not found to be associated with the number of people present, whereas self-rated elation was positively correlated with the presence of others. Multiple regression analyses suggested that the presence of other people facilitates intake and increases elation independently. It also suggested that social facilitation operates by independently increasing the size and the duration of meals and that it operates independently of the subjective state of the individual. These results contradict the predictions of increased arousal, increased hunger, and increased emotionality models but support attentional, disinhibitory, and time extension models of social facilitation.

Metabolic rate and feeding behavior.

According to the ischymetric hypothesis, hunger is induced by the decrease of overall metabolic rate. In order to assess such a mechanism, it was necessary to monitor the muscular contraction-free metabolic rate designated "métabolisme de fond" (MF) in rats that were either resting or moving. MF was then examined in relation to either spontaneous or induced feeding patterns. A computerized open-circuit gas analysis system allowed us to monitor MF and behavior and to show that the onset of a spontaneous meal was preceded by a decrease of MF and its termination is preceded by a rebound of MF. Pharmacological blockade of utilization of both glucose and lipids enhanced feeding only to the extent that it reduced MF. These findings apply to pharmacotherapy because the anorexigenic effect of dexfenfluramine results from the enhancement of MF induced by the capacity of this drug to mobilize endogenous fat reserves and to so provide an endogenous meal that inhibits the exogenous meal. The ischymetric mechanism of hunger does not exclude important modulatory input from hormonal, circadian, and environmental factors in the control of feeding.

Spontaneous meal patterns of humans: influence of the presence of other people

Social influences on eating were investigated by paying 63 adult humans to maintain 7-d diaries of everything they ingested, time, subjective hunger, and number of people present. Meals eaten with others contained more carbohydrate, fat, protein, and total calories; had smaller deprivation ratios; and had larger satiety ratios than meals eaten alone. The number of people present was positively correlated with meal size even when meals eaten alone were excluded. Adding the number of people present as a factor in a multiple-regression prediction of meal size more than doubled the variance accounted for, without altering the influence of other predictors, suggesting that social factors are associated independently with an increase in meal size. Meal size was positively correlated with the postmeal interval for meals eaten alone but not for meals eaten with other people. This suggests that social factors increase amounts eaten and disrupt postprandial regulation.

Brief intraportal infusion of pancreatic glucagon reduces spontaneous meal size in rats

Brief intraportal infusion of pancreatic glucagon reduces spontaneous meal size in rats

Gastric distention by balloon and test-meal intake in obese and lean subjects

A study was conducted to determine the effects of various levels of gastric distension on spontaneous meal intake. A balloon was inserted into the stomach of four lean and four obese subjects before consumption of a lunch meal. On different days the balloon was filled with 0, 200, 400, 600, and 800 mL water in a random sequence. As balloon volume increased, food intake decreased, with a balloon volume of greater than or equal to 400 mL significantly reducing intake (p less than 0.01). There was no significant difference between lean and obese subjects. Because gastric emptying rate was not significantly slowed by a volume of 800 mL, between emptying was probably not a factor in inducing satiety. Discomfort was probably also not a factor because it was experienced by only two lean subjects at 800 mL. Most likely gastric distension itself triggered satiety signals.

Measuring Feed Intake Patterns and Meal Size of Lactating Dairy Cows

Length, size, and interval between eating bouts were determined for four forages with two lactating dairy cows. The forages were 1) low dry matter alfalfa haylage, 2) high dry matter alfalfa haylage, 3) alfalfa hay, and 4) alfalfa pellets. Recordings were made for 96-h periods, and nibbling bouts were separated from meals according to the time and weight of eating bouts. Meal data were analyzed by a stepwise least squares analysis to determine the best model for characterizing feed intake data for lactating dairy cows. Initial meal size and lengths were not different; however, interval following the initial meal was longer on the alfalfa pellet diet. Spontaneous meals were similar in number and size for all diets; however, meal length was increased on the alfalfa hay diet.Total daily dry matter intakes were not different for the four diets. It is important to distinguish between nibbling and meals for effective analysis of intake, feeding behavior, and meal patterns.

Circadian rhythms of the spontaneous meal pattern, macronutrient intake, and mood of humans

Circadian (24-hour) rhythms in the feeding behavior of humans were investigated using diary self-reports of spontaneous food intake. Eight male and 30 female undergraduate students recorded what they ate, when they ate it, and their mood at the time of ingestion in a diary over a consecutive nine day period. Self-ratings of depression, energy, and anxiety were made at the beginning of each meal on three seven-point scales. The total amount of food energy in each meal as well as the amount of protein, carbohydrate, and fat, the intervals prior to and following the meals, and the satiety and deprivation ratios were calculated. The food energy contained in the stomach at the beginning and end of each meal was estimated with a mathematical model. These variables were evaluated in relation to the time of meal occurrence during the day. Fluctuations in the levels of self-rated energy and anxiety, but not depression, were detected during the day. Clear 24-hour rhythms were identified for the amount eaten and the macronutrients ingested during the day with decreases for males and increases for females. The amount eaten per meal and the meal's content of carbohydrate or fat, but not protein, varied over the day with peaks at the lunch and dinner periods. A clear sex difference without circadian variation was apparent with the deprivation ratios. This suggests that males eat larger meals than females because of a heightened responsivity to deprivation and not to a smaller response to the satiating properties of food. Preprandial correlations were found for meals occurring either during the breakfast or the dinner periods. No postprandial correlations were found. These data demonstrate that the preprandial correlations are not an artifact produced by the 24-hour rhythm and suggests that they reflect a basic regulatory strategy employed by humans. As the day progressed, postmeal intervals and satiety ratios decreased, while premeal intervals increased. This suggests that humans obtain less satiety from a given amount of food later in the day than earlier. It is postulated that this represents eating which anticipates the overnight fast. These data clearly demonstrate the efficacy of the approach and the orderly, analyzable nature of the spontaneous eating behavior of humans.