Intestinal satiety in rats.

In 5 experiments with a total of 55 male Sprague-Dawley rats, infusion of liquid food into the duodenum inhibited sham feeding. The inhibition reflected satiety because the duodenum infusion elicited the complete behavioral sequence characteristic of satiety. The chemical and/or colligative load that the infusion imposed on the intestine appeared to be the adequate stimulus for satiety. Duodenal infusions that inhibit sham feeding and elicit satiety are not aversive, because they will not function as the UCS for the formation of a conditioned taste aversion for saccharin. The satiety elicited by the infusion of food into the duodenum is termed "intestinal satiety" by the authors. This emphasizes the belief that satiety is a reflex that can be elicited by the activation of receptors in the wall of the intestine. It is known that the activation of some intestinal receptors releases the hormone cholecystokinin (CCK). Since CCK mimics a duodenal infusion by inhibiting sham feeding and eliciting the complete behavioral sequence of satiety, it is suggested that CCK mediates intestinal satiety in the rat. (21 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Satiety and behavioral caloric compensation following intragastric glucose loads in the rat.

Administered glucose solutions intragastrically to male Sprague-Dawley albino rats having free access to food except during the 1st hr. after intubation. The distribution of meals after intubation indicated that effects of glucose both prolong satiety and contribute to its initiation, during the dark or the bright phase of the lighting cycle. From about 5 hr. after intubation and from the start of the 2nd meal, the net cumulative inhibition of food intake amounted to apparently close to exact caloric compensation for the glucose load. Feeding was not differentially inhibited by control loads of the same volume as the glucose load, whether the control was air, water, sodium chloride, urea, or 3-methylglucose. Results provide the 1st demonstration in support of a theory of short-term behavioral regulation according to an energostatic signal generated from glucose. (48 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Fluid intake and behavioral changes in rats associated with the distension of the small and large intestine.

Effects of volumetric distension of the small and the large intestine on rats' behavior were compared. Rats were stimulated by a rubber balloon inserted into chronic isolated intestinal loops prepared from the lower duodenum-upper jejunum and from the upper colon in the same animal. Thresholds of 3 reaction classes (weak, strong, and painful) were not different from each other in the 2 loops. Distension decreased fluid intake in an intensity-dependent way, with weak and painful stimuli being less effective in the large intestine and strong stimuli less effective in the small bowel. Behavioral indexes supported intake data, satiety indexes were similar to each other and changed in time, whereas aversivity indexes differed in the 2 loops and as a function of intensity but not time. The author suggests that mild discomfort is a physiological satiety factor whereas strong and painful stimuli signal danger and induce aversivity. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cholecystokinin elicits the complete behavioral sequence of satiety in rats.

Observed and scored the behavior of intact rats and rats with chronic gastric fistulas during a 60-min test period when they were offered liquid diet after 17 hr of food deprivation. The same 5 adult male Sprague-Dawley rats were employed in 2 experiments. Intact Ss and Ss with closed fistulas displayed a specific behavioral sequence at the end of each meal: They stopped eating, engaged in grooming and exploration for a short time, and then rested or slept. Thus, a fixed behavioral sequence characterized satiety in Ss. Although the behavioral sequence of satiety was fixed, the cessation of feeding was not a sufficient condition for the appearance of the rest of the sequence: Quinine adulteration of the liquid diet stopped sham feeding but did not elicit the complete sequence. Intraperitoneal injection of the intestinal hormone cholecystokinin during sham feeding, however, elicited the complete sequence of satiety. The observation that cholecystokinin not only stopped feeding but elicited the complete sequence of satiety supports the hypothesis that endogenous cholecystokinin is a satiety signal for the rat. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Absence of satiety during sham feeding in the rat.

In 2 experiments, a total of 9 Sprague-Dawley rats with chronic gastric fistulas were trained to eat a liquid diet. Results indicate that when the fistulas were opened for the first time, Ss sham-fed eagerly and did not become satiated during test periods of 2 or 7.5 hrs. This sustained hyperphagia occurred after long (17 hrs) or short (10-30 min) intermeal intervals. The experience of sustained hyperphagia when gastric fistulas were open did not affect intake of the same diet on the next day when gastric fistulas were closed. When taste and other oropharyngeal stimuli acted alone during sham feeding, they did not elicit satiety. It is concluded that the occurrence of satiety in rats is critically dependent on an inhibitory reflex elicited by ingested food accumulating in the stomach and moving through the small intestine. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Unlearned appetite controls: Watersnakes (Nerodia) take smaller meals when they have the choice.

Studies of appetite in mammals emphasize that meal size is learned, but lactation and parental care constrain testing of naive individuals. Neonatal reptiles, in contrast, are self-sufficient foragers. The authors examined the effect of prey size on meal size in primivorous (at first feeding) northern watersnakes (Nerodia sipedon). When offered an excess of small prey (2%-20% of snake mass), neonates ate significantly smaller meals (M = 23.5% of snake mass) than when offered a single huge item (range = 32%-55%). The authors conclude that (a) the taking of smaller meals is not a learned effect, (b) there may be a satiety threshold for meal size rather than a target, (c) oropharyngeal stimuli may provide satiety cues, and (d) huge meals may have fitness costs. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Peripheral control of drinking: Gastrointestinal filling as a negative feedback signal, a theoretical and experimental analysis.

Conducted 5 experiments to investigate the hypothesis that the osmotic postingestional satiety signal proposed by R. A. McCleary (1953) operates through a mechanism related to gut filling rather than by osmotically induced shifts of fluid from osmoreceptors in the brain. Ss were a total of 15 male albino Sprague-Dawley rats and 31 Charles River rats. A control theory model, designed to make quantitatively explicit the hypothesis under question, is presented. Results show that when mannitol, which is not absorbed from the intestine, is added to a highly palatable saccharin-glucose mixture, the amount of fluid consumed decreased in inverse proportion to the mannitol concentration. Mannitol blocked fluid absorption from the intestine at a low concentration and at higher concentrations to lead to a net flux of fluid into the intestinal lumen. It was also shown that mannitol in concentrations that reduced the intake of the palatable solution did not induce thirst when Ss were in water balance. It did induce thirst when Ss were tested in a state of negative water balance. Results, considered as a whole, support the view that McCleary's osmotic postingestional satiety signal acts as an intestinal distention signal rather than by inducing thirst. (48 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of ovariectomy on meal pattern in the albino rat.

In a study with 24 female albino Sherman rats, it was found that after ovariectomy most Ss increased food intake while continuing to eat discrete meals. Meal size increased in ovariectomized Ss, whereas meal frequency decreased. It is suggested that ovariectomy impairs the onset of satiety during a meal but not the ability to regulate total intake through modification of intermeal interval. (21 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Intravenous injections of cholecystokinin and caerulein suppress food intake in domestic fowls

As with various mammals, cholecystokinin (CCK) and caerulein have short-term, dose-related, inhibitory effects on feeding when injected i.v. in domestic fowls. It is estimated that in meals lasting more than about 6 min there could be time for ingested food to reach the duodenum and for the release of CCK to act as a satiety signal.     

The influence of thermic effect of food on satiety

OBJECTIVES: To evaluate energy expenditure after three isoenergetic meals of different nutrient composition and to establish the relationship between the thermic effect of food (TEF), subsequent energy intake from a test meal and satiety sensations related to consumption. DESIGN: The study employed a repeated measures design. Ten subjects received, in a randomized order, three meals of 2331+/-36 kJ (557+/-9 kcal). About 68% of energy from protein in the high protein meal (HP), 69% from carbohydrate in the high carbohydrate meal (HC) and 70% from fat in the high fat meal (HF). SETTING: The experiments were performed at the University of Milan. Subjects: Ten normal body-weight healthy women. METHODS: Energy expenditure was measured by indirect calorimetric measurements, using an open-circuit ventilated-hood system; intake was assessed 7h later by weighing the food consumed from a test meal and satiety sensations were rated by means of a satiety rating questionnaire. RESULTS: TEF was 261+/-59, 92+/-67 and 97+/-71 kJ over 7 h after the HP, HC and HF meals, respectively. The HP meal was the most thermogenic (P < 0.001) and it determined the highest sensation of fullness (P=0.002). There were no differences in the sensations and thermic effect between fat and carbohydrate meals. A significant relationship linked TEF to fullness sensation (r=0.41, P=0.025). Energy intake from the test meal was comparable after HP, HC and HF meals. CONCLUSIONS: Our results suggest that TEF contributes to the satiating power of foods.     

Mathematical analysis of energy regulatory patterns of normal and diabetic rats.

Analysis of feeding patterns indicated that diabetic (alloxan) hyperphagia is characterized by doubling of meal sizes with no change in feeding frequency. 10 normal and 10 diabetic male Long-Evans rats were used. Correlation of meal sizes and intermeal intervals did not provide any systematic relationships for either normal or diabetic Ss. When equations of the general form Y = A + Bcos(X) were fit to successive satiety ratios (postmeal interval-meal size), diabetic Ss showed significantly lower A coefficients, reflecting a lower average level of satiety, as well as significantly lower B coefficients, reflecting less systematic variability in the satiating value of food around the average level. It is concluded that the major regulatory deficit in diabetic animals is a chronic reduction in the long-term signal of body nutrient repletion. (19 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Food for thought: a critique on the hypothesis that endogenous cholecystokinin acts as a physiological satiety factor

This review evaluates the various lines of evidence supporting the hypothesis that cholecystokinin (CCK) released from the small intestine during feeding plays a physiological satiety. Issues considered include, the effects of systemic injection of CCK on consummatory and operant feeding, the role of the vagus nerve, the effects of CCKB receptor antagonists, and the neuroendocrine responses to exogenous CCK. A critical appraisal of this research indicates that while it is clearly demonstratable that exogenous peripheral CCK can alter food intake by acting on CCKA receptors, the mechanism involved may be more closely related to the induction if aversion and nausea, rather than satiety. With regard to peripheral endogenous CCK, the available evidence also does not seem to support a role for the hormone in satiety. In particular, it is doubtful whether plasma concentrations of CCK following a meal are sufficiently high to inhibit feeding. Moreover, CCKA receptor antagonist which do not cross the blood brain barrier fail to increase meal size, as would be expected if peripheral CCK was an effective satiety factor. In addition, the recent literature concerned with the possibility that CCK may have a direct action within the brain in the control of food intake has been reviewed. These studies show that CCK administered intracerebroventicularly, or by micoinjection into discrete brain regions, also inhibits feeding via a CCKA receptor mechanism. However, the physiological relevance of these findings have yet to be determined.     

Failure by deprived hamsters to increase food intake: Some behavioral and physiological determinants.

Investigated the behavioral and physiological determinants of postfast anorexia in 165 golden hamsters. Six experiments varied the postfast feeding in photoperiods, feeding in different hamster strains, the effects of a liquid diet, Ss' adaptation to a restricted water schedule, food intake as a function of housing, and physiological changes during food deprivation. Postfast anorexia and/or the failure to adapt to a feeding schedule were not restricted to a particular photoperiod condition or hamster strain. The anorexia was also observed with a liquid diet, but Ss showed large increases in water intake on a water deprivation schedule. When Ss were group-housed, they pouched food during scheduled feeds and ate it later: Meal size was not increased. Measures of gastric fill and plasma metabolites indicated that filling and emptying of the forestomach occurred with a periodicity similar to that of spontaneous meals; data are consistent with strong peripheral satiation/satiety mechanisms in this species. (31 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Contribution of gastric and postgastric feedback to satiation and satiety in women

Two parallel preload studies were conducted to determine the relative contributions of inhibitory feedback from the stomach and intestine to satiation (meal termination) and postprandial satiety. In the Gastric Emptying Study, five normal-weight women each ingested an egg sandwich (307 kcal) (1) immediately after a tomato soup preload (120 kcal), (2) 20 min after a tomato soup preload, and (3) with no preload. There was 125 g more of soup in the stomach when subjects began ingesting the sandwich immediately compared to 20 min after the soup, and the emptying of the sandwich was delayed when it was ingested immediately but not 20 min after the soup. The lag times for emptying of the sandwich were 76.5 (69.1-82.4), 47.2 (20.1-67.7), and 42.4 (17.8-65.1) min for the three conditions, respectively, p < 0.05. In the Food Intake Study, 16 normal-weight women ate significantly less (p < 0.01) in test meals offered immediately (978+/-246 kcal) and 20 min (1027+/-298 kcal) after the soup preload than in a test meal with no preload (1151+/-279 kcal). Despite the different amounts of soup in the stomach, subjects' test-meal intake in the two preload conditions was not significantly different. Subjects' fullness ratings following the preloads and the test meals were not different among the treatment conditions. The results suggest that feedback from neither the gastric nor the postgastric compartment is primary in determining meal size and postprandial satiety. Instead, signals from gastric and postgastric sources are combined to determine meal size and postprandial satiety.     

Either a paradigm shift or no mental measurement: the nonscience and the nonsense of The Bell Curve

We have shown previously that intravenous infusions of insulin, known to induce glucoprivic hunger, and of insulin combined with glucose, known to induce satiety, produce in the VMH and PVN of Wistar rats monoaminergic changes that differ from those related to spontaneously occurring hunger and satiety, while the genetically obese Zucker rat is totally resistant to the behavioural effects of insulin and insulin + glucose infusions. In the present study, the impact of these infusions on VMH and PVN monoamines in obese Zucker rats was assessed using microdialysis. Monaminergic changes (increase in DOPAC and 5-HIAA and decrease in DA and 5-HT) were quite similar in obese rats to those we found in normal rats when insulin was infused. In contrast, changes in 5-HT or DA in response to insulin and glucose were quite different in the Zucker rat. Monoaminergic changes related to meals were more dramatic in the Zucker rat and so were able to reverse the background changes produced by the insulin infusion. These data confirm the idea that the effect on monoamines of spontaneously occurring hunger and satiety is different from the effect on monoamines by insulin and glucose-induced hunger and satiety. The results show disturbances of the obese Zucker rat related both to insulin and to hypothalamic monoamines that may be involved in the hyperphagia and obesity of this model.     

Injections into the duodenum and the induction of satiety in the rat.

Examined ways in which the intestine might participate in the induction of satiety, using direct intestinal injections to alter the contents of the duodenum and then observing the effect on subsequent food intake over a 21/2-hr period. Ss were 24 male hooded rats, food-deprived for approximately 17 hr. The injection of either bulk or hypertonic solutions (NaCl or glucose) into the duodenum suppressed food intake. The injection of substantial amounts of food did not have an effect greater than that caused by equivalent amounts of nonnutritive bulk and the injection of acid material did not suppress eating more than basic material. These results suggest that bulk and osmotic pressure in the duodenum may initiate physiological changes which can ultimately participate in the regulation of meal size but that metabolites, duodenal hormones, and specific dynamic action do not. With the gastrointestinal system intact, the flow of material from the stomach to the intestine would be sufficiently slow that neither changes in duodenal bulk nor osmotic pressure would be involved in the regulation of meal size. When the stomach is partially removed or denervated, the rate of passage of food into the duodenum may increase enough so that osmotic and bulk signals originating in the duodenum would help to regulate meal size. (French summary) (33 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Hyperpolarization of the liver cell membrane by palmitate as affected by glucose and lactate: implications for control of feeding

Since the membrane potential of liver cells being in contact with vagal afferents has been proposed to represent a major signal in metabolic control of food intake, we investigated the effect of palmitate, glucose and lactate on the membrane potential of hepatocytes with microelectrodes using superfused mouse liver slices. The mice used for the experiments were fed a fat-enriched diet (18% fat). Palmitate (0.5 mM) hyperpolarized the membrane of hepatocytes by 3-4 mV, and this hyperpolarization was not affected by 5-10 mM glucose and 0.5-1 mM lactate. Glucose alone did not influence the potential, even when mice fed a high carbohydrate diet were employed. At lactate concentrations > or = 2 mM the palmitate induced hyperpolarization was eliminated and 5 mM lactate or pyruvate alone hyperpolarized the liver cell membrane. Similar to the palmitate induced hyperpolarization, the lactate induced hyperpolarization was prevented by the K-channel blocker TEA, suggesting that activation of K channels is involved in the hyperpolarization. The results show that physiological concentrations of glucose and lactate do not affect the hyperpolarization of the liver cell membrane due to fatty acid oxidation. The implications of these findings with regard to control of food intake by fatty acid oxidation and lactate metabolism are discussed. The observations are consistent with a signal function of the hepatic membrane potential in physiological control of food intake by fatty acid oxidation. Hepatic lactate metabolism at supraphysiological lactate concentrations may also produce a satiety signal coded by the hepatic membrane potential.     

Human salivary sugar clearance after sugar rinses and intake of foodstuffs

Effects of chronic intraluminal amylase inhibition on eating and the digestive system are unclear. In growing rats, we determined the effect of ingesting a wheat amylase inhibitor (AI) on eating, weight, small intestinal mucosal growth, and disaccharidases. Three groups of 12 rats received AI, were pair-fed controls (PFC), or had free access to food (FAC). After measuring food intake and body and stool weight for 21 d, rats were decapitated and the small intestine was divided into four segments. AI and PFC rats had similar food intake, weight gain, and stool output, but these were less than FAC rats (P < 0.005). AI rats ate less (P < 0.001) than PFC during the light cycle and less than FAC rats during darkness. Mucosal DNA and RNA were reduced (P < 0.05) in the upper small intestine of AI and PFC rats compared with FAC rats. Mucosal weight, RNA, and disaccharidase activities were greater (P < 0.01) in the ileum of AI rats compared with PFC and FAC rats. AI alters the amount and pattern of food intake, reduces weight gain, upper small intestinal mucosal weight, protein and DNA, and increases distal small intestinal mucosal weight, RNA, and disaccharidases. AI likely causes these effects by inducing satiety and increasing carbohydrate delivery to the distal intestine.     

Role of signals for unconditioned stimulus absence in the sensitivity of autoshaping to contingency.

Pigeons autoshape to a keylight conditioned stimulus (CS) that is poorly correlated with a food unconditioned stimulus (UCS) if UCSs occurring in the absence of the CS are signaled by some other cue. Three experiments examined if this is because signaling blocks context conditioning or because it converts the intertrial interval (ITI) into a predictor of UCS absence. Results indicated that cuing periods of UCS absence was not sufficient for acquisition. Signaling failed to produce acquisition if the signal also accompanied the CS, although this procedure converts the ITI into a predictor of UCS absence. The detrimental effect of compounding the signal with the CS occurred only if the signal was separately paired with the UCS, which suggests it was due to blocking of the CS by the signal. The results suggested that the signaling effect depends on blocking of the context by the signal, not on conversion of the ITI into a signal for UCS absence. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Mother's milk: A determinant of the feeding preferences of weaning rat pups.

Studied feeding preferences of weaning rat pups in 4 experiments with 20 recently parturate female hooded rats and their litters (reduced to 8 or 12 pups per litter). Results show that cues associated with the diet eaten by a lactating female rat are transmitted to her young, probably via her milk, and are sufficient to markedly influence the food preferences of her young during weaning. For their 1st meals of solid food, the weanlings actively seek and preferentially ingest the diet their mother has been eating during the nursing period, even if that diet is relatively unpalatable. (15 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)