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Query: UMLS:C0020175 (hunger)
 5,670 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The control of feed intake is highly complex, involving many peripheral, as well as central nervous system (CNS) factors. The various signals involved in the control of feeding behavior are integrated in the hypothalamus and appropriate responses, i.e., feeding or cessation of feeding, are generated. The actual neurochemical events subserving this function are not well understood, although specific roles for each of the neurotransmitter systems have been proposed. More recently, certain neuropeptides have been shown to affect feeding behavior in sheep, as well as many other species. Most of the evidence points to the involvement of two families of neuropeptides in the control of feed intake in sheep: the opioid peptides, which include enkephalins, endorphins and dynorphins, and cholecystokinin (CCK) peptides, of which CCK-8 is the primary brain form. Certain opioid peptides, such as met-enkephalins, beta-endorphin and dynorphin A peptides, have been shown to stimulate feeding after CNS administration in sheep, while CCK peptides suppress feeding. Thus it has been proposed that opioid peptides are involved in the initiation of feeding, or hunger, and CCK peptides, in the inhibition of feeding, or satiety. Although much more is known about the effects of CCK peptides than opioid peptides on feeding behavior of sheep, evidence is accumulating for direct interaction between CCK- and opioid-containing neurons that could lead to better understanding of hunger and satiety in sheep.
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PMID:Control of feed intake in sheep. 615 Sep 29

The effects of cholecystokinin octapeptide sulfate ester (CCK-8-SE) and unsulfated cholecystokinin (CCK-8-NS) were studied following intraventricular administration on active avoidance and conditioned feeding behaviour of rats. In the CCK-8-NS and CCK-8-SE treated animals the acquisition of active avoidance and conditioned feeding behaviour were considerably impaired compared to the control; furthermore, these peptides caused a facilitated extinction of active avoidance and conditioned feeding behaviour. The data suggest that cholecystokinin octapeptide is capable of modifying the fear and hunger motivated behaviours of rats.
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PMID:Effects of intraventricular administration of cholecystokinin octapeptide sulfate ester and unsulfated cholecystokinin octapeptide on active avoidance and conditioned feeding behaviour of rats. 628 48

The evidence for the participation of signals from the gastrointestinal tract in hunger and satiety is reviewed. Various methods of subjecting only certain portions of the gastrointestinal tract to food are described including sham feeding, crossing of the intestines of two animals, and intragastric, intraduodenal and intravenous feeding. These methods have revealed that animals eat more when only the mouth is exposed to food, but consume less when food enters the stomach directly and still less when feeding themselves intravenously. The role of the stomach in satiety is discussed in relation to the results of the many experiments in which intragastric loads were administered. These experiments generally revealed that gastric loads suppressed intake in proportion to their caloric value, but that compensation was not precise. A similar analysis is made of the role of the intestines in satiety. These studies present evidence for osmoreceptors and glucoreceptors, distention, and pressure, all of which may participate in satiety. The numerous effects of vagotomy on food intake are reviewed and an attempt is made to separate afferent from efferent effects and vagal effects from nonspecific surgical injury. The role of other afferents is explored. A brief survey of the most recent studies on humoral factors indicates that cholecystokinin is probably acting as a satiety agent, but its mode of action remains unknown. The changes in the gastrointestinal tract that accompany an increase or decrease in food intake reveal adaptive changes that occur in the organ. The evidence for gastrointestinal factors in satiety of the suckling animal is presented. Finally, a hypothesis is presented in which the various factors that bring a meal to an end are included. Preabsorptive satiety may consist of multiple factors which probably include signals from osmoreceptors and possibly other chemoreceptors in the upper small intestine. The signals from these receptors are neural while other products of digestion stimulate the release of humoral agents, such as cholecystokinin, which may act locally, in the liver, or on the central nervous system. Stretch or distention of the intestines at various locations may also contribute to preabsorptive satiety.
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PMID:Gastrointestinal factors in hunger and satiety. 628 33

Cholecystokinin octapeptide (CCK-OP) was reported to decrease the intake of liquid food in lean and in obese man. This study investigated the effect of CCK-OP on the consumption of real life food, i.e., of standardized sandwiches. Sixteen young non-obese females and males participated, after an overnight fast, each in two experiments. After a basal 30 min, saline or CCK-OP, 1.5 or 3.0 Ivy Dog Units/kg body weight/15 min, was infused in random double blind fashion, while sandwiches were placed in front of the subjects. For the next three 15-min periods, the subjects were instructed to eat as much as they liked. In the first 15 min after 3.0 as well as 1.5 U CCK-OP/kg/15 min significantly fewer sandwiches (50 and 17 percent) were eaten than after saline (p less than 0.01 and p less than 0.05) and less hunger was reported (p less than 0.02 and p less than 0.05). Self-reported activation decreased only with 3.0 U CCK-OP (p less than 0.005). Reports of well-bring , electroencephalogram, heart rate, and respiration were not altered. The results support the notion that CCK is involved in the regulation of food intake.
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PMID:Cholecystokinin octapeptide decreases intake of solid food in man. 628 18

The paper presents studies of the influence of octapeptide cholecystokinin (ChCK-8) on the level of dofamine, noradrenaline and serotonine in the hypothalamus, septum, amygdala, striatum and mesencephalon of the rats brain during 24-, 48- and 96-hour alimentary and water deprivation. A change of catecholamines content under the influence of ChCK-8 was observed for the most part in conditions of thirst and only in the hypothalamus. ChCK-8 action in conditions of water deprivation was selective and directed mainly to the restoration of the changes in transmitter's level. ChCK-8 did not have a significant influence on the level of the brain monoamines during hunger. It may be assumed, that "satiation" hormone ChCK-8 is to a great extent connected with the mechanisms of reinforcement, and its "satiating" effect would appear at catecholamines' level in the process of satisfying of corresponding need.
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PMID:[Effect of cholecystokinin octapeptide on brain monoamine levels during feeding and drinking motivational excitation]. 631 87

Because controversy exists as to the interpretation of the known feeding-suppressive effects of various neuropeptides, we attempted to construct a model that could differentiate satiety from other nonspecific effects. Reasoning that a satiety factor should be less inhibiting of feeding in a hungrier animal, whereas aversive agents should be unaffected by hunger, we studied the neuropharmacologic dose responses of five substances administered peripherally to rats at two different degrees of starvation. Included were four neuropeptides with putative satiety effects: cholecystokinin, calcitonin, bombesin, and pancreatic polypeptide, as well as the known aversive agent lithium chloride. In the study, cholecystokinin behaved as we postulated a satiety factor would, showing significant effect of starvation at every dose and in the ANOVA. The aversive agent lithium showed overlapping among the starvation groups and no starvation effect by ANOVA. Calcitonin failed to show differences attributable to starvation. Bombesin produced some overlapping of starvation groups and a barely significant starvation effect by ANOVA. Pancreatic polypeptide produced no feeding suppression in the rat. We conclude that cholecystokinin is a short-term satiety signal and that calcitonin acts peripherally by some nonspecific nonsatiating means. Bombesin's effects are unclear but may be nonspecific.
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PMID:Are peptides truly satiety agents? A method of testing for neurohumoral satiety effects. 666 Mar 34

Using combined immuno-staining and retrograde tracing techniques many of the ascending visceral and taste pathways within the rat central nervous system have been shown to be composed of a variety of neuropeptide and catecholamine synthesizing enzyme containing neurones. The pathway we examined extended from the periphery to sensory cortex and included: the nodose ganglion (periphery)----solitary nucleus (medulla)----parabrachial nucleus (pons)----ventral posterior medial nucleus (thalamus)----visceral and taste sensory areas (cortex). In the solitary nucleus of the medulla many neuronal cell bodies could be shown to be both immuno-positive for one of 6 neuropeptides including avian pancreatic peptide (APP), cholecystokinin (CCK), enkephalin (ENK), neurotensin (NT), somatostatin (SOM) and substance P (SP) or the catecholamine synthesizing enzyme tyrosine hydroxylase (TOH) and to have a projection to the parabrachial nucleus of the pons. In the parabrachial nucleus of the pons many neuronal cell bodies could be shown to be immuno-positive for one of 5 neuropeptides (CCK, ENK, NT, SOM, SP) and have a projection to the ventral posterior medial nucleus of the thalamus. In the ventral posterior medial nucleus of the thalamus several neuronal cell bodies were shown to be immuno-positive for one of 3 neuropeptides (CCK, ENK, SOM) and project to the visceral and taste sensory cortex. This is the first report of neuropeptides being present in the projection neurones of any sensory system in the central nervous system and for the first time describes an entire set of putative neurotransmitters which extends from the periphery to the sensory cortex. From previous studies it also appears that in all cases examined the relevant receptors are present in these visceral and taste relay nuclei in order for the neuropeptide or catecholamine to produce an effect upon release. Comparisons between rat and other animals suggest that a similar organization of these visceral and taste pathways may also be present in other mammals including man. Functionally these neuropeptides containing projection neurones appear to be primarily involved in relaying visceral information rather than taste information. In this capacity activation of these neurones may produce such visceral sensations as malaise, well being, hunger, satiety or thirst.
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PMID:Neuropeptides are present in projection neurones at all levels in visceral and taste pathways: from periphery to sensory cortex. 673 52

Many peptides are contained in specific cells distributed throughout the gastrointestinal tract. Some are known to be released by the presence of specific components of food and to affect specific gastrointestinal functions related to digestion and absorption of nutrients. For many of the more recently identified peptides, however, stimuli for release and physiological functions are unknown. Improved radioimmunoassay techniques have allowed measurement of serum concentration changes of peptides that act via endocrine but not neurocrine or paracrine modes of action. Peptides that may play a role in the control of food intake include cholecystokinin (CCK), bombesin (BBS) and pancreatic polypeptide (PP) as possible satiety components and opiates as possible hunger components. All four have been found in the brain as well as in the gastrointestinal tract. Systemic administration of each has been shown to affect food intake, but whether doses used produced changes that normally occur during a meal awaits further development of radioimmunological assays. In the obese, the decreased sensitivities to, or decreased concentrations of the satiety components CCK, BBS and PP and the increased concentrations of the hunger component, B-endorphin, may contribute to the imbalance of food intake and energy expenditure, which leads to the accumulation of adipose tissue.
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PMID:Role of peptides from gastrointestinal cells in food intake regulation. 676 31

Cholecystokinin decreases food intake in animals and in man. This study investigated whether the structurally related ceruletide reduces food intake in healthy non-obese man. Twelve females and 12 males participated, after an over-night fast, in each of two experiments. During the basal 40 min, saline was infused IV. Thereafter, the infusion was, in random double blind fashion, either continued with saline or switched to 60 or 120 ng/kg b. wt/hr ceruletide. Butter was melted in a pan and scrambled eggs with ham were prepared in front of the subjects, who were instructed to eat, together with bread and mallow tea, as much as they wanted. With 120 ng/kg/hr ceruletide, the subjects ate significantly less (16.8 percent) than with saline (3725 kJ +/- 489 SEM and 4340 kJ +/- 536, respectively; p less than 0.025). They also reported less hunger (p less than 0.005) and activation (p less than 0.005) and activation (p less than 0.01), and had longer reaction times (p less than 0.01) and a weaker psychomotor performance (p less than 0.025). 60 ng/kg/hr ceruletide decreased food intake only slightly (6.6%; 3089 kJ +/- 253 and 3292 kJ +/- 300 respectively) and no significant changes in the above measures occurred. In conclusion, ceruletide reduces food intake in man, thus resembling the effects of cholecystokinin.
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PMID:Ceruletide decreases food intake in non-obese man. 713 28

Rats eat more at night than during the day. This work investigated whether this nocturnal hyperphagia is characterized by increased hunger, decreased postprandial satiety, or both. Rats were presented with liquid food after 3-hr food deprivation at the midpoint of the night or day phase of a 12:12 hr light/dark cycle. Quinine adulteration of food produced equal percentage suppression of first meal size (MS) and of 60-min intakes in the night and the day. This suggests that rats are equally hungry after 3-hr food deprivation in the night and the day. In contrast to apparently equal hunger, rats were less satiated by ingested food after 3 hr of food deprivation at night than during the day. This conclusion is based on the observations that the postprandial intermeal interval (IMI) was significantly shorter at night and that the satiety ratio (IMI/MS) was smaller at night. This nocturnal decrease in the satiating potency of ingested food was demonstrated for two specific preabsorptive satiety mechanisms: (a) the pregastric satiety mechanism(s) stimulated by sham feeding and (b) cholecystokinin, the putative satiety hormone released by food contacting the mucosal surface of the upper small intestine. All the results suggest that the diurnal variation of food intake in rats is primarily the result of diurnal variation in the potency of postprandial satiety mechanisms.
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PMID:Nocturnal hyperphagia in the rat is characterized by decreased postprandial satiety. 736 7


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