Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 5 year period, eight patients in whom acute acalculous cholecystitis developed during intravenous hyperalimentation are reviewed with emphasis on factors contributing to pathogenesis. Gallbladder distention, biliary stasis, and bile inspissation, thought to be important in the pathogenesis of this disease, are enhanced with the use of hyperalimentation, and this potential complication is being seen with increasing frequency in seriously ill or injured patients who are being fed parenterally. In addition to hyperalimentation, sepsis, hypotension, multiple transfusions (more than 10 units), prolonged fasting, and ventilatory support were frequent common denominators. Typical findings of pain, tenderness, and a mass in the right upper abdominal quadrant are infrequent, and the diagnosis rests on a high index of suspicion and ultrasonography. This syndrome may be preventable by the stimulation of gallbladder emptying with intermittent fat ingestion or parenteral infusion of cholecystokinin.
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PMID:Acute acalculous cholecystitis: a complication of hyperalimentation. 11 61

The hyperphagia characteristic of some types of obesity may result from a deficiency in one or more components of the systems controlling satiety which in rats may include the gastrointestinal hormone cholecystokinin (CCK). Obesity may also influence responsivity to often used central nervous system (CNS)-acting drugs and combination of drugs. In these experiments it was shown that: (1) Zucker fatty rats were less sensitive than lean to intraperitoneal injections of 20 U/kg CCK after a 6-hr fast and when reduced were less sensitive than lean and less sensitive than when obese to injections of 5 U/kg CCK; (2) Although fatties were equally sensitive as leans to injections of 0.5 and 1.0 mg/kg d-amphetamine sulfate, when reduced, they were less sensitive; (3) Injections of 1.25 and 2.5 mg/kg diazepam produced smaller increases in food intake after a 6-hr fast in fatty and reduced fatty than lean rats; (4) Combination of diazepam with cholecystokinin in both fatty and lean rats produced feeding similar to that following injection of carrier; and (5) A similar additive effect was obtained in both fatty and lean rats when diazepam was combined with amphetamine; however, the fatty appeared to be more sensitive to the amphetamine than the diazepam effect. Thus the Zucker fatty rat appears to be less sensitive to these chemicals which affect food intake, which supports the contention that their CNS is generally less responsive.
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PMID:Cholecystokinin, amphetamine and diazepam and feeding in lean and obese Zucker rats. 44 Oct 98

Peripheral administration of the COOH-terminal octapeptide of cholecystokinin in doses from 1 to 100 micrograms per kilogram of body weight (0.25 to 25.0 micrograms per rat) significantly antagonized tail pinch-induced eating in rats, an animal model for stress-induced human hyperphagia. Centrally administered cholecystokinin was effective only in high doses (3 micrograms into the cerebral ventricle). The finding that the minimal effective dose of cholecystokinin in suppressing stress-induced appetitive behavior is smaller after peripheral than central administration suggests that the peptide is acting on peripheral, as opposed to central nervous system, substrates.
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PMID:Cholecystokinin inhibits tail pinch-induced eating in rats. 56 35

Extracts of the cerebral cortes of genetically obese (ob/ob) mice with hyperphagia contain 0.05 +/- 0.02 microgram (mean +/- standard error) of cholecystokinin octapeptide equivalent per gram of wet weight compared to 0.15 +/- 0.01 microgram per gram for their nonobese littermates and 0.20 +/- 0.01 microgram per gram for normal LAF1 mice. These findings are suggestive of a causal relation between the diminished brain immunoreactive cholecystokinin content and the unrestrained appetite of the obese mice.
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PMID:Cholecystokinin in the brains of obese and nonobese mice. 75 80

The intestinal hormone cholecystokinin (CCK) elicits satiety in rats and inhibits food intake in rhesus monkeys. This behavioral effect is specifically related to the C-terminal octapeptide structure of CCK and is a new biological effect of the hormone. Endogenous CCK released by food entering the duodenum may inhibit feeding and elicit satiety under physiological conditions, but no experimental evidence is availabe on this point. Until such evidence becomes available, we believe that CCK should be considered a putative satiety signal. The satiety effect of CCK suggests a therapeutic role of CCK for human hyperphagia and obesity. An interesting therapeutic alternative to administration of exogenous CCK is the release of endogenous CCK by nutrients such as amino acids. These nutrients can be ingested as preloads which are calorically trivial, but which release significant amounts of CCK. Such preloads inhibit food intake in rhesus monkeys. Their efficacy in man has not been determined.
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PMID:Cholecystokinin: a putative satiety signal. 122 92

This paper updates the informations on the three most important anorexigenic peptides: cholecystokinin, neurotensin and corticotropin-releasing factor. Their peripheral and/or central effects on food and water intakes as well as on dietary preferences are detailed. Their mechanisms of action and regulation are examined. This includes the interactions with classical neurotransmitters (norepinephrine, dopamine, etc...) as well as the description of the brain nuclei and neuronal networks involved. Finally, their variations in disturbed feeding behavior (hyperphagia, anorexia) in man or in animal models are reviewed.
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PMID:[Cholecystokinin, neurotensin and corticotropin-releasing factor, three important anorexic peptides]. 144 78

Contraction of the gallbladder is mediated through the release of cholecystokinin from duodenal cells secondary to enteral feedings. Premature infants are often nourished by parenteral hyperalimentation leading to prolonged inactivation of the gallbladder. Such inactivation probably accounts for the increased incidence of gallbladder distention observed in premature neonates. Two cases of premature infants are described in whom distention of the gallbladder occurred during parenteral hyperalimentation. The distention resolved spontaneously secondary to the introduction of enteral feedings. A trial period of oral or tube feeding is recommended in such cases prior to any attempt to release the distention by a surgical intervention.
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PMID:Gallbladder distention in premature neonates receiving parenteral nutrition. 251 31

The aim of this investigation was to study the release of cholecystokinin (CCK) in connection with feeding and lactation and to investigate the involvement of CCK in the regulation of food intake. For this purpose a method based on high performance liquid chromatography and subsequent radioimmunoassay (RIA) for the determination of CCK in plasma was developed. CCK was also determined in the cerebrospinal fluid (CSF) by RIA and is referred to as CCK-like immunoreactivity (CCK-LI). Different molecular forms of CCK in dog and rat plasma have been determined. These were found to differ from those in the CSF, suggesting that the CCK measured in plasma and CSF are derived from different sources, i.e. the gut and brain. CCK was released into plasma in response to feeding in dogs and rats and in response to suckling in lactating animals. The release of CCK is under vagal control. Thus, electrical vagal stimulation of anaesthetized rats increased plasma levels of CCK, and abdominal vagotomy abolished the suckling-induced release of CCK. Lesions of the lateral midbrain, which disrupt the oxytocin-mediated milk-ejection reflex, were also found to block the increase in plasma CCK in response to suckling. Intraperitoneal (i.p.) injection of CCK octapeptide (CCK-8) decreased food intake in food deprived male rats in doses which resulted in plasma concentrations within the physiological range. Intracerebral, but not i.p., injection of a low dose of a CCK antagonist, reversed the effect of peripheral CCK-8 on food intake as did i.p. injection of peripheral CCK A receptor antagonists. Thus, the mechanism by which i.p. CCK-8 inhibits food intake may involve both peripheral and central CCK receptor mechanisms. The concentration of CCK-LI in the CSF decreased after food deprivation and increased after feeding or i.p. CCK-8. Intraperitoneal injection of peripheral CCK antagonists prevented the increase in CCK-LI in the CSF and the inhibitory effect of i.p. CCK-8 on food intake. These data indicate that peripheral CCK receptor mechanisms induce a release of CCK in the brain. During the hyperphagia of lactation, plasma but not CSF levels of CCK were increased in the rat. Food deprivation markedly decreased the concentration of CCK in plasma and CSF; and the levels were restored in CSF, but not in plasma, after 1 h of feeding. Removal of the litter decreased food intake and increased the concentration of CCK in the CSF, but not in plasma. Lactating rats were less sensitive to the inhibitory effect of i.p.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of cholecystokinin in feeding and lactation. 260 47

Children with Prader-Willi syndrome (PWS) are characterized by obesity, hyperphagia, hypogonadism, and mental retardation with underlying hypothalamic dysfunction and are known to have blunted or absent pancreatic polypeptide (PP) secretion in response to protein meals. In this communication, adults (26 +/- 3 years of age) with PWS were compared with age-matched normal obese and normal weight controls in regards to plasma glucose, insulin, PP, cholecystokinin (CCK), cholesterol, and triglyceride after a high protein meal. Compared with normal weight controls, adults with PWS showed a smaller and delayed rise in plasma insulin, and relatively smaller and delayed PP elevation whereas obese controls revealed hyperglycemia, markedly higher insulin, and moderately higher PP, cholesterol, and triglyceride levels than those with PWS. There was a small increment of CCK levels after a protein meal in all groups of adults. After a protein meal, the molar ratio of PP to CCK doubled in normal weight and PWS groups, and this ratio tripled in the normal obese group, suggesting no reduced PP secretion in PWS in response to CCK stimulation. PP hyposecretion in PWS thus appears to be a part of multiple endocrinopathy associated with hypothalamic dysfunction.
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PMID:Protein meal-stimulated pancreatic polypeptide secretion in Prader-Willi syndrome of adults. 266 31

The strengths of taste aversion induced by sulphated cholecystokinin 26-33 (CCK-8; 1,2,4 and 8 micrograms/kg IP) and lithium chloride (LiCl; 7.5, 15, 30 and 60 mg/kg IP) were determined in order to assess the relative aversiveness of the two compounds. All doses of LiCl induced strong aversion, but only the highest dose of CCK-8 induced aversion, which was mild. Effects of CCK-8 and LiCl on food intake were then compared in the hour (hr) following 8 hr of food deprivation; rats were on this food deprivation schedule for a relatively long time (78 days) throughout testing. All doses of CCK-8 reduced food intake significantly. Most doses of LiCl either did not affect or significantly increased food intake. Although 60 mg/kg LiCl did not affect food intake when administered 15 or 30 min before food presentation, it significantly increased food intake when administered 1, 2 or 3 hr before food presentation. Overeating of solid food may be an illness-induced behavior. Although a very high dose of LiCl (120 mg/kg) decreased food intake markedly, the rats were obviously distressed, not satiated. Failure of CCK-8 to affect feeding behavior like LiCl is indirect evidence that the reduction of food intake by CCK-8 is not merely the result of aversiveness, but is an extremely potent and specific behavioral effect.
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PMID:Cholecystokinin octapeptide and lithium produce different effects on feeding and taste aversion learning. 301 Mar 48


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