The effects of ration level on food retention time in juvenile lemon sharks,Negaprion brevirostris

Synopsis Fecal production was monitored to observe the effects of meal size on retention time of food in the digestive tracts of lemon sharks, Negaprion brevirostris. Initial appearance of feces occurred more rapidly when ration level was increased. The onset of fecal production was negatively correlated with rate of intake. Production of feces continued for a longer period of time when meal size was increased. Retention time of food was directly related to feeding rate, suggesting that the rate of digestion was constant. The correlation between retention time and intake on a percentage body weight basis was greater than the correlation between retention time and intake on an energy density basis. The use of agar to bind food may have delayed digestion and prolonged food passage for sharks fed an experimental diet.     

Salmon calcitonin reduces food intake through changes in meal sizes in male rhesus monkeys

Amylinergic mechanisms are believed to be involved in the control of appetite. This study examined the effects of the amylin agonist, salmon calcitonin, on food intake and meal patterns in adult male rhesus monkeys. Fifteen minutes before the onset of their 6-h daily feeding period, monkeys received intramuscular injections of various doses of salmon calcitonin (0.032, 0.056, 0.1, 0.32, and 1 microg/kg) or saline. Salmon calcitonin dose dependently reduced total daily and hourly food intake, with significant decreases at the 0.1, 0.32, and 1 microg/kg doses. Daily food intake was reduced by approximately 35%, 62%, and 96%, at these doses, respectively. An analysis of meal patterns revealed that size of the first meal was significantly reduced across the dose range of 0.056 to 1 microg/kg, while average meal size was reduced with the 0.32 and 1 microg/kg doses. Meal number was only affected at the 1 microg/kg dose. Repeated 5-day administration of the 0.1 microg/kg dose resulted in a reduction in daily food intake only on injection day 2, while significant reductions in food intake were observed on all five injection days with a 0.32 microg/kg dose. Daily food intake was also reduced for 1 day after the termination of the 5-day injections of the 0.32 microg/kg salmon calcitonin dose. These sustained reductions in intake were expressed through decreases in meal size. These data demonstrate that salmon calcitonin acutely and consistently decreases food intake mainly through reductions in meal sizes in nonhuman primates.     

Increased short-term food satiation and sensitivity to cholecystokinin in neurotrophin-4 knock-in mice

Neurotrophin-4 (NT-4) knockout mice exhibited decreased innervation of the small intestine by vagal intraganglionic laminar endings (IGLEs) and reduced food satiation. Recent findings suggested this innervation was increased in NT-4 knock-in (NT-4KI) mice. Therefore, to further investigate the relationship between intestinal IGLEs and satiation, meal patterns were characterized using solid and liquid diets, and cholecystokinin (CCK) effects on 30-min solid diet intake were examined in NT-4KI and wild-type mice. NT-4KI mice consuming the solid diet exhibited reduced meal size, suggesting increased satiation. However, compensation occurred through increased meal frequency, maintaining daily food intake and body weight gain similar to controls. Mutants fed the liquid diet displayed a decrease in intake rate, again implying increased satiation, but meal duration increased, which led to an increase in meal size. This was compensated for by decreased meal frequency, resulting in similar daily food intake and weight gain as controls. Importantly, these alterations in NT-4KI mice were opposite, or different, from those of NT-4 knockout mice, further supporting the hypothesis that they are specific to vagal afferent signaling. CCK suppressed short-term intake in mutants and controls, but the mutants exhibited larger suppressions at lower doses, implying they were more sensitive to CCK. Moreover, devazepide prevented this suppression, indicating this increased sensitivity was mediated by CCK-1 receptors. These results suggest that the NT-4 gene knock-in, probably involving increased intestinal IGLE innervation, altered short-term feeding, in particular by enhancing satiation and sensitivity to CCK, whereas long-term control of daily intake and body weight was unaffected.     

Circadian rhythms of food intake in gastroduodenally-ulcerated rats: effects of three anti-ulcer drugs

The effects of three anti-ulcers drugs on the temporal distribution of food intake and of the two parameters, meal size and meal frequency, were studied in ulcerated and non-ulcerated rats exposed to light-dark (LD 12:12) cycles. Experimental ulceration with indomethacin reduces the amplitude of meal frequency and brings the acrophase forward, compared with non-ulcerated animals. These effects were reversed by the oral administration of either ranitidine, sucralfate or pirenzepine along with the food. However, the administration of either pirenzepine or sucralfate alone to non-ulcerated rats is accompanied by significant (P less than 0.05) changes in the circadian patterns of meal size and meal frequency without the total daily food intake being affected in any way (pirenzepine treatment caused large intake of food during the light period while sucralfate treatment resulted in marked food intake during the dark period). The results indicate that circadian modification of meal patterns in the ulcerated rats are attributable to indomethacin-induced gastrointestinal mucosal injury and anti-ulcer medications.     

Continuous infusion of cholecystokinin and meal pattern in the rat

Purified natural cholecystokinin (CCK-33) was infused continuously for two days at a rate of 5.9 μg/hr in two rats trained to bar-press for food (Noyes pellet 45 mg) on a fixed ratio of five bar presses to obtain one pellet. The animals also received control surgery and were tested in the operant chamber for two days, one prior to and the other following the CCK-33 treatment. CCK-33 suppressed the number of meals, the total amount of food eaten, and the total duration of time spent eating. However, the size of each meal and the rate of intake were not affected. The CCK effect did not interact with the light-dark phases of diurnal cycle. It appears that a major effect of continuous systemic elevation of CCK-33 is to reduce food intake by prolonging the satiety period rather than by decreasing the individual meal size.     

The GLP-1 agonist exendin-4 reduces food intake in nonhuman primates through changes in meal size

Exendin-4 (Ex4), a long-acting glucagon-like peptide-1 (GLP-1) receptor agonist, has been shown to reduce food intake and suppress gastric emptying in rodents and humans. In this study we investigated the effects of peripheral administration of Ex4 on food intake and meal patterns in adult male rhesus macaques. Rhesus macaques (n = 4) that had been trained to lever press for food pellets were injected intramuscularly 15 min before the start of their 6-h daily feeding period. Ex4 was given at doses of 0.10, 0.32, 0.56, 1.0, and 3.0 microg/kg. Ex4 suppressed food intake in a dose-dependent manner, with the 3.0 microg/kg dose completely preventing feeding during the 6-h period and the 0.10 microg/kg dose suppressing intake by 17%. Doses of 0.32, 0.56, 1.0, and 3.0 microg/kg caused significant reductions in cumulative intake at all six hourly time points. Ex4 inhibited food intake through a specific effect on meal size. Meal size was significantly reduced in a dose-dependent manner with significant reductions at the 0.32 and 1.0 microg/kg doses (P < 0.05). Day 2 and 3 intakes returned to baseline levels with no compensation for Ex4-induced feeding suppression. Administration of doses of 0.32 and 0.56 microg/kg Ex4 over 5 consecutive days led to sustained reductions in intake with no evidence of compensation. Again, these reductions were due to specific effects on meal size. These results demonstrate that activation of GLP-1 pathways has potent effects on the controls of meal size and overall food intake in a nonhuman primate model.     

Effect of i.c.v. infusion of the alpha-MSH agonist MTII on meal patterns in male rats following nicotine withdrawal

The present study explored the role of endogenous alpha-MSH in the alteration of meal patterns induced by nicotine (NIC) withdrawal. Male Sprague Dawley rats bearing third ventricle cannulas were placed in computerized food intake monitors. On days 1-21, the rats were given 4 mg/kg/day of NIC or saline (SAL) in four equal i.p. doses during the dark period. NIC suppressed (P < 0.05) food intake only during the first week. The normalization of food intake occurred when the reduced meal size of the NIC injected rats was countered by an increase in meal number. Despite the normalization of 24-h food intake, body weight in NIC rats was decreased (P < 0.05) for 21 days. On day 22, the rats were divided into 4 groups (n's = 7-8 each) and injected into the third ventricle with various doses of the alpha-MSH agonist MTII or artificial cerebrospinal fluid (aCSF): SAL + aCSF, SAL + MTII, NIC + aCSF, NIC + MTII. Infusion of MTII (30 ng/rat) suppressed (P < 0.01) dark phase food intake in both groups, but the NIC + MTII group ate (P < 0.05) more than the SAL + MTII group. Meal number during the dark phase was suppressed by MTII, but the NIC + MTII group took significantly more meals that the SAL + MTII group. Infusion of MTII suppressed meal size in SAL and NIC treated rats, but this effect was attenuated in NIC treated rats. All meal parameters normalized by the day after i.c.v. infusion. These data indicate that NIC treatment differentially affects the neural controls of meal number and meal size and attenuates the suppression by MTII of meal number and meal size.     

Evidence for the role of hindbrain orexin-1 receptors in the control of meal size

Hypothalamic orexin neurons project to the hindbrain, and 4th-ventricle intracerebroventricular (4th-icv) injection of orexin-A treatment increases food intake. We assessed the effects of hindbrain orexin-A and the orexin-1-receptor antagonist SB334867 on meal pattern in rats consuming standard chow. When injected 4th-icv shortly before dark onset, lower doses of orexin-A increased food intake over a 2-h period by increasing the size of the first meal relative to vehicle, whereas the highest dose increased food intake by causing the second meal to be taken sooner. Conversely, hindbrain SB334867 reduced food intake by decreasing the size of the first meal of the dark phase. We also examined the effects of 4th-icv orexin-A and SB334867 on locomotor activity. Only the highest dose of orexin-A increased activity, and SB334867 had no effect. In addition, hindbrain SB334867 induced c-Fos in the nucleus of the solitary tract. These data support the suggestion that endogenous hindbrain orexin-A acts to limit satiation. Both orexin-A and the pancreatic satiation hormone amylin require an intact area postrema to affect food intake, so we asked whether 4th-icv orexin-A impairs the satiating effect of peripheral amylin treatment. Amylin reduced the size of the first meal of the dark cycle when rats were pretreated with 4th-icv saline, yet amylin was ineffective after 4th-icv orexin-A pretreatment. Using double-label immunohistochemistry, we determined that some orexin-A fibers in the area postrema are located in proximity to amylin-responsive neurons. Therefore, hindbrain orexin-A may increase food intake, in part, by reducing the ability of rats to respond to amylin during a meal.     

The pattern of feeding of first instar nymphs of Schistocerca americana

ABSTRACT The feeding behaviour of nymphs Schistocerca americana (Drury) was recorded throughout the light phases of the first stadium using a behavioural event recording program on a microcomputer. Most food was ingested on day 4 of the stadium, very little on day 1 and none on day 6, the final day of the stadium. Only 26–45% of the total food intake over the stadium occurred during the dark periods and more food was eaten in the last 4 h of each light period than earlier. Feeding occupied only about 5% of the total time. Variation in food intake was a consequence primarily of changes in the numbers of meals. After day 1, the average meal size did not change significantly. Meal length increased relatively slightly compared with meal size as a consequence of an increase in the proportion of time spent feeding in each meal as meal size increased. Meal size was correlated with the length of the previous interfeed suggesting a volumetric regulation. The distribution of pauses within meals was also consistent with the thesis that meal size is governed by the level of excitation in the central nervous system at the start of the meal.     

Evidence for the effect of tryptophan on the pattern of food consumption in free feeding and food deprived rats.

The effects of injections of 50 mg/kg L-tryptophan upon meal size, meal frequency, rate of eating and satiety ratios were measured in rats whose feeding behaviour was monitored continuously over 24-h periods. A number of precautions were taken to minimize the effects of novel or stressful experimental procedures, to prevent the contamination of behaviour during periods of data collection and to maximise the detection of subtle effects on behaviour. In freely-feeding rats tryptophan brought about a significant diminution in the 24-h food intake and significantly reduced meal size. When food deprived rats were tested under similar circumstances tryptophan significantly reduced the size of the first large meal taken after the deprivation period and markedly extended the duration of the post-meal interval. The conditions adopted in this study to improve the sensitivity of the behavioural assay for feeding have made possible the detection of certain small but clear effects of tryptophan on food consumption in rats.     

Amylin receptor blockade stimulates food intake in rats

Amylin is postulated to act as a hormonal signal from the pancreas to the brain to inhibit food intake and regulate energy reserves. Amylin potently reduces food intake, body weight, and adiposity when administered systemically or into the brain. Whether selective blockade of endogenous amylin action increases food intake and adiposity remains to be clearly established. In the present study, the amylin receptor antagonist acetyl-[Asn(30), Tyr(32)] sCT-(8-32) (AC187) was used to assess whether action of endogenous amylin is essential for normal satiation to occur. Non-food-deprived rats received a 3- to 4-h intravenous infusion of AC187 (60-2,000 pmol.kg(-1).min(-1)), either alone or coadministered with a 3-h intravenous infusion of amylin (2.5 or 5 pmol.kg(-1).min(-1)) or a 2-h intragastric infusion of an elemental liquid diet (4 kcal/h). Infusions began just before dark onset. Food intake and meal patterns during the first 4 h of the dark period were determined from continuous computer recordings of changes in food bowl weight. Amylin inhibited food intake by approximately 50%, and AC187 attenuated this response by approximately 50%. AC187 dose-dependently stimulated food intake (maximal increases from 76 to 171%), whether administered alone or with an intragastric infusion of liquid diet. Amylin reduced mean meal size and meal frequency, AC187 attenuated these responses, and AC187 administration alone increased mean meal size and meal frequency. These results support the hypothesis that endogenous amylin plays an essential role in reducing meal size and increasing the postmeal interval of satiety.     

Brain stem melanocortinergic modulation of meal size and identification of hypothalamic POMC projections

Metabolic, cognitive, and environmental factors processed in the forebrain modulate food intake by changing the potency of direct controls of meal ingestion in the brain stem. Here, we behaviorally and anatomically test the role of the hypothalamic proopiomelanocortin (POMC) system in mediating some of these descending, indirect controls. Melanotan II (MTII), a stable melanocortin 4 receptor (MC4R) and melanocortin 3 receptor (MC3R) agonist injected into the fourth ventricle near the dorsal vagal complex, potently inhibited 14-h food intake by decreasing meal size but not meal frequency; SHU9119, an antagonist, increased food intake by selectively increasing meal size. Furthermore, MTII injected into the fourth ventricle increased and SHU9119 tended to decrease heart rate and body temperature measured telemetrically in freely moving rats. Numerous alpha-melanocyte-stimulating hormone-immunoreactive axons were in close anatomical apposition to nucleus tractus solitarius neurons showing c-Fos in response to gastric distension, expressing neurochemical phenotypes implicated in ingestive control, and projecting to brown adipose tissue. In retrograde tracing experiments, a small percentage of arcuate nucleus POMC neurons was found to project to the dorsal vagal complex. Thus melanocortin signaling in the brain stem is sufficient to alter food intake via changing the potency of satiety signals and to alter sympathetic outflow. Although the anatomical findings support the involvement of hypothalamomedullary POMC projections in mediating part of the descending, indirect signal, they do not rule out involvement of POMC neurons in the nucleus tractus solitarius in mediating part of the direct signal.     

Temporal patterning of feeding by hummingbirds

For five species of hummingbirds in the laboratory, time between meals was related to energy intake on the first meal and rate of energy expenditure between meals. Field observations gave similar results. Average meal sizes were similar at one intake rate independent of food caloric density; females averaged longer bouts than males. When rate of intake was approximately halved, meal duration approximately doubled and volume intake remained similar. We postulate that feeding is initiated when crop contents reach a lower threshold and that feeding is terminated after ingestion of an optimal volume determined by the added weight of the meal.     

Hyperphagia and obesity in OLETF rats lacking CCK-1 receptors

The brain-gut peptide cholecystokinin (CCK) inhibits food intake following peripheral or site directed central administration. Peripheral exogenous CCK inhibits food intake by reducing the size and duration of a meal. Antagonist studies have demonstrated that the actions of the exogenous peptide mimic those of endogenous CCK. Antagonist administration results in increased meal size and meal duration. The feeding inhibitory actions of CCK are mediated through interactions with CCK-1 receptors. The recent identification of the Otsuka-Long-Evans-Tokushima Fatty (OLETF) rat as a spontaneous CCK-1 receptor knockout model has allowed a more comprehensive evaluation of the feeding actions of CCK. OLETF rats become obese and develop non-insulin dependent diabetes mellitus (NIDDM). Consistent with the absence of CCK-1 receptors, OLETF rats do not respond to exogenous CCK. OLETF rats are hyperphagic and their increased food intake is characterized by a large increase in meal size with a decrease in meal frequency that is not sufficient to compensate for the meal size increase. Deficits in meal size control are evident in OLETF rats as young as 2 days of age. OLETF obesity is secondary to the increased food intake. Pair feeding to amounts consumed by intact control rats normalizes body weight, body fat and elevated insulin and glucose levels. Hypothalamic arcuate nucleus peptide mRNA expression in OLETF rats is appropriate to their obesity and is normalized by pair feeding. In contrast, pair fed and young pre-obese OLETF rats have greatly elevated dorsomedial hypothalamic (DMH) neuropeptide Y (NPY) mRNA expression. Elevated DMH NPY in OLETF rats appears to be a consequence of the absence of CCK-1 receptors. In intact rats NPY and CCK-1 receptors colocalize to neurons within the compact subregion of the DMH and local CCK administration reduces food intake and decreases DMH NPY mRNA expression. We have proposed that the absence of DMH CCK-1 receptors significantly contributes to the OLETF's inability to compensate for their meal size control deficit leading to their overall hyperphagia. Access to a running wheel and the resulting exercise normalizes food intake and body weight in OLETF rats. When given access to running wheels for 6 weeks shortly after weaning, OLETF rats do not gain weight to the same degree as sedentary OLETF rats and do not develop NIDDM. Exercise also prevents elevated levels of DMH NPY mRNA expression, suggesting that exercise exerts an alternative, non-CCK mediated, control on DMH NPY. The OLETF rat is a valuable model for characterizing actions of CCK in energy balance and has provided novel insights into interactions between exercise and food intake.     

Meal pattern of male rats maintained on histidine-, leucine-, or tyrosine-supplemented diet

Objective: Food intake is known to be affected by macronutrient composition of the diet, and protein manipulation has been reported to alter food intake, but the effect of individual amino acids on eating behavior has not been fully studied. This study investigated the effect of diet supplementation with three individual amino acids on meal pattern in male rats. Research Methods and Procedures: Thirty‐two Sprague‐Dawley rats were randomly divided into four equal groups and fed control diet or histidine (5%)‐, leucine (5%)‐, or tyrosine (5%)‐supplemented diet for 2 weeks and were monitored for their meal pattern. Results: Total food intake and feeding rate of the different groups were not affected, although other components of meal pattern were altered. Histidine supplementation reduced diurnal meal size by 42% (p < 0.05), whereas that of leucine increased nocturnal meal size by ～35% (p < 0.05). Tyrosine supplementation increased food intake of the nocturnal period and decreased that of the diurnal period. Both histidine and tyrosine supplementation elevated fasting plasma insulin levels and suppressed fasting glucose significantly. Discussion: Individual amino acids were found to alter meal pattern differently. Further investigations are required to dissect the involvement of central and peripheral factors in these alterations.     

The effect of stomach fullness on food intake of whiting in the North Sea

The probability of a North Sea whiting Merlangius merlangus stomach containing fresh food was depressed when partially digested food was already present in the stomach. The lowered probability was detected even at levels where the fish was physiologically able to ingest an average meal. The feeding probability of c . 15% of the fish caught was predicted to be severely decreased at the level of partially digested food found in the stomachs. No effect of stomach fullness on meal size was found, indicating that the saturation is affecting search activity rather than prey or meal size selection. The diurnal pattern in food intake varied between the five sampling locations, presumably as a result of differences in prey availability.     

The short term satiety peptide cholecystokinin reduces meal size and prolongs intermeal interval

Camostat mesilate (or mesylate) releases endogenous cholecystokinin (CCK) or CCK-58, the only detectable endocrine form of CCK in the rat, and reduces cumulative food intake by activating CCK₁ receptor. However, the literature lacks meal pattern analysis and an appropriate dose-response curve for this peptide. Therefore, the current study determines meal size (MS), intermeal interval (IMI) and satiety ratio (SR) by orogastric gavage of camostat (0, 12.5, 25, 50, 100, 200, 300, 400, 800 mg/kg) and compares them to those previously reported by a single dose of CCK-8 (1 nmol/kg, i.p), the most utilized form of CCK. We found that camostat (200, 300, 400 and 800 mg/kg) and CCK-8 reduced cumulative food intake and the size of the first meal, but only camostat prolonged IMI and increased SR. There was no change in the duration of the first two meals or in rated behaviors such as feeding, grooming, standing and resting in response to camostat and CCK-8, but there was more resting during the IMI in response to camostat. This study provides meal pattern analysis and an appropriate dose-response curve for camostat and CCK-8. Camostat reduces food intake by decreasing MS and prolonging IMI, whereas CCK-8 reduces food intake by reducing only meal size.     

Nicotine's attenuation of body weight involves the perifornical hypothalamus

Previously we showed that intermittent administration of nicotine (NIC) in the dark phase decreased food intake and body weight and this could be blocked when the NIC receptor antagonist mecamylamine was infused into the fourth ventricle. Catecholaminergic neurons adjacent to the fourth ventricle contain NIC receptors and directly innervate the perifornical hypothalamus (PFH) which has been shown to be involved in regulation of feeding. This study explored whether NIC regulates feeding behavior by modulating catecholaminergic input to the PFH. Epinephrine and norepinephrine neuronal input was ablated within the PFH by infusion of 6-hydroxydopamine hydrobromide (6-OHDA), while bupropion was infused to protect dopaminergic neurons. After recovery of body weights to pre-surgery levels, food intake, meal size, meal number and body weight were measured after intermittent NIC injections. The results showed the PFH lesioned animals did not exhibit the typical prolonged drop in food intake, meal size and body weight normally associated with NIC administration. High performance liquid chromatography analyses demonstrated that compared to control rats, 6-OHDA administration significantly reduced PFH norepinephrine and epinephrine levels, but not dopamine levels. These results are consistent with NIC reducing food intake in part by acting through catecholaminergic neurons within or extending through the PFH.     

Peptide YY(3-36) inhibits gastric emptying and produces acute reductions in food intake in rhesus monkeys

Peptide YY3-36 [PYY(3-36)], a gastrointestinal peptide that is released into the circulation in response to ingesting a meal, has recently been suggested to play a role in controlling food intake. PYY(3-36) has been reported to inhibit food intake following peripheral administration in rodents and in human subjects. To more fully characterize the potential feeding actions of PYY(3-36), we examined the ability of a dose range of PYY(3-36) (0.3-3.0 nmol/kg) to affect liquid gastric emptying and daily 6-h food intake in male rhesus monkeys. Intramuscular PYY(3-36) produced a dose-related inhibition of saline gastric emptying that was maximal at a dose of 3 nmol/kg. Intramuscular PYY(3-36) administered before daily 6-h food access produced significant feeding reductions at doses of 1 and 3 nmol/kg. Analyses of the patterns of food intake across the 6-h period of food access revealed that PYY(3-36) increased the latency to the first meal and reduced average meal size without altering meal number. Although single doses of PYY(3-36) reduced intake, a suppressive effect on food intake was not sustained over multiple administrations across successive days. Together, these data suggest that PYY(3-36) has the ability to reduce food intake in acute test situations in nonhuman primates. Whether this is a physiological action of the endogenous peptide remains to be determined.     

Influence of eating modalities on water intake in dog (author's transl)]

Food and water intake of a dog which had free access to water were studied in three experimental circumstances: 1) Food given ad libitum. 2) Food given at fixed hours. 3) Food deprivation for four days followed by resumption of food intake. A) The results indicate the water intake follows a pattern, the profile, range and duration of which can be modified within 24 hrs. In spite of modifications related to food intake, a typical profile remains which suggests that water is taken according to a program which is at least partly indepdent of food intake. B) Under experimental condition 1, food and water intake were weakly related, probably revealing an acquired relationship between the meal weight and the water intake which immediately precedes and follows food intake. The correlation was strengthened when the dog was forced to eat only once a day (observation 2). On the contrary, after a period of starvation (observation 3) the previous relationship between meal weight and water intake lessens and others appear which suggest the action of direct mechanisms of shortage compensation as far as water and food are concerned.