Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether exogenous cholecystokinin (CCK) and endogenous CCK evoke different gastrointestinal motor responses, we investigated the motility induced by CCK by use of standard manometric methods. Injection (ip) of 500 ng/kg CCK caused immediate profound gastric inhibition and duodenal phasic excitation that did not resemble the postprandial pattern. Similar profound gastric inhibition has been associated with nausea. The contribution of endogenous CCK to the fed pattern of motility was investigated using proglumide; intraperitoneal injection of the antagonist before feeding caused no change, but injection before a second meal induced a decrease (P less than 0.025, n = 6) in gastric pressure with no accompanying duodenal change. This suggests that CCK causes an increase in gastric pressure that could result from a delay in gastric emptying. In support of this hypothesis, we have previously demonstrated, by use of proglumide, that endogenous CCK delays gastric emptying. Therefore exogenous CCK may reduce food intake by evoking an abnormal gastrointestinal motor pattern that may induce malaise, whereas endogenous CCK may decrease food intake by delaying gastric emptying, thus prolonging gastric satiety signals.
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PMID:Endogenous and exogenous cholecystokinin may reduce food intake by different mechanisms. 361 36

Administration of cholecystokinin (CCK) to rats caused a dose-dependent increase in plasma levels of the neurohypophyseal hormone oxytocin (OT). The OT secretion was comparable to that found in response to nausea-producing chemical agents that cause learned taste aversions. The effect of CCK on OT secretion was blunted after gastric vagotomy, as was the inhibition of food intake induced by CCK. Food ingestion also led to elevated plasma OT in rats, but CCK and aversive agents caused even greater OT stimulation. Thus, after administration of large doses of CCK, vagally mediated activation of central nausea pathways seems to be predominantly responsible for the subsequent decrease in food intake. Despite their dissimilar affective states, both nausea and satiety may activate a common hypothalamic oxytocinergic pathway that controls the inhibition of ingestion.
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PMID:Oxytocin secretion in response to cholecystokinin and food: differentiation of nausea from satiety. 371 53

A review of the satiating effect of cholecystokinin in humans reveals that the synthetic C-terminal octapeptide of cholecystokinin (CCK-8) inhibits liquid and solid food intake in non-obese men and women, and in obese men. Side effects, such as nausea, slight stomach sickness or abdominal cramps are infrequent and transient, and they are neither necessary nor sufficient for the inhibition of intake. These results demonstrate the efficacy of the satiating effect of CCK-8 in humans. The therapeutic potential of CCK-8 cannot be estimated until further studies are performed that demonstrate the efficacy of CCK-8 for decreasing body weight and that the safety of CCK-8 when it is administered repetitively for prolonged periods is established.
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PMID:The therapeutic potential of cholecystokinin. 610 Jan 12

Sincalide, the C-terminal octapeptide fragment of the cholecystokinin, was used to contract the gallbladder during routine oral cholecystography in 18 patients. In 14 patients clinically important contraction occurred. The average reduction in gallbladder size for these patients was 32.7% of the preinjection size (range 15.1%-67.9%). Within 8-12 minutes cystic duct visualisation occurred in 8 and common bile duct visualisation in 3 patients. Spasm of the gallbladder neck was found in 2 cases. The blood pressure and heart rate did not change significantly during the study. Six patients felt slight nausea for 1-4 minutes and two vomited. We conclude that sincalide may be useful in biliary tract function studies in special clinical conditions (i.e. upper abdominal pain with unknown aetiology).
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PMID:The effect of intravenously administered sincalide on the human gallbladder during oral cholecystography. 630 54

The irritable bowel syndrome (IBS) is clinically characterized by a wide variety of symptoms, including dyspepsia, flatulence, nausea, cramping abdominal pain, constipation and/or diarrhea, and nonspecific symptoms, probably reflecting autonomic nervous system overreactivity. Physiologically, the colonic motor abnormality is characterized by an altered slow-wave rhythm, quantitative differences from normal in the repetitive contraction pattern of the rectosigmoid area, and increased colonic muscle responsiveness to hormones such as cholecystokinin and pentagastrin. The diagnosis of IBS involves practical and ethical considerations as well as the need for decisive reassurance of the patient through judicious examination. Treatment of IBS requires a thoughtful and sensitive approach to the patient, recognition of IBS as an important clinical problem, regularization of bowel function, relief of the abdominal discomfort, and intelligent emotional support.
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PMID:The irritable bowel syndrome. A clinical review and ethical considerations. 701 25

Mild tail pinch (TP) in rats resulted in 72% of animals displaying ingestive behavior with 20% demonstrating gnawing behavior without food ingestion and 8% demonstrating licking behavior only. The animals ate steadily over 5 min with a maximum rate occurring at 1 min (0.5 +/- 0.2 g). There was a circadian rhythm of TP-induced behavior with the peak food ingestion occurring at 24 h. A mild increase in blood glucose occurred 120 s after commencement of TP (115 +/- 4 mg/dl). Common satiety signals such as stomach distension and glucose decreased food ingestion. Parenteral administration of glucagon, cholecystokinin-octapeptide, bombesin, and thyrotropin-releasing hormone resulted in suppression of TP-induced food ingestion. Chronic TP (12 5-min TP periods/day) resulted in a fall in spontaneous food intake with the total intake remaining similar to food intake prior to the chronic TP period. We suggest that TP serves as an excellent model for eating behavior because 1) it correlates well with starvation-induced eating; 2) it precludes the necessary deprivation of food and water to adrenalectomized animals; and 3) animals subjected to TP continue chewing in the face of decreased food intake allowing one to exclude the possibility that the effects of an anorectic are secondary to nausea.
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PMID:Stress-induced eating in rats. 719 55

To investigate the hypothesis that peripherally administered cholecystokinin (CCK) reduces food intake by the production of aversive internal cues, we examined the effects of the sulfated, octapeptide form of CCK on taste reactivity responses to oral sucrose infusions in male rats implanted with intraoral cannulas. After injection of CCK (4, 8, or 16 micrograms/kg ip) or 0.15 M saline (1 ml/kg ip), a series of brief (30 s) intraoral infusions of a 0.30 M sucrose solution was administered at 2-min intervals for 10 min. All doses of CCK were found to significantly decrease ingestive responding during the first and subsequent sucrose infusions without promoting a significant increase in aversive responses relative to controls. The lack of a gradual, conditioned shift in taste reactivity responses, from an ingestive to an aversive pattern (which is typically observed after LiCl administration), suggests that the production of nausea-like aversive internal cues was likely not responsible for the observed CCK-induced alterations in taste reactivity responses. It appears that the unconditioned, satiogenic effects of CCK contributed to the selective reduction in ingestive responses observed in the present study.
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PMID:Cholecystokinin reduces sucrose palatability in rats: evidence in support of a satiety effect. 781 Jul 58

There is evidence to suggest that the arginine vasopressin release observed in association with emesis after i.v. injection of cholecystokinin (CCK) and N-methyl-D-aspartate (NMDA) is mediated by stimulation of emetic centers in the brainstem. That the GnRH-releasing action of NMDA is also sometimes accompanied by emesis led to the suggestion that stimulation of this parvocellular system by the glutamate agonist may also be mediated in part via activation of brainstem pathways. If this is the case, then other nauseogenic agents, such as CCK, should similarly elicit GnRH release. The foregoing prediction was tested in the castrated juvenile male monkey, an experimental model characterized by the absence of spontaneous GnRH release. GnRH discharges were monitored indirectly by measuring changes in circulating LH concentrations after the responsivity of the gonadotroph had been heightened by a chronic intermittent i.v. infusion of the decapeptide. An i.v. bolus of CCK at 10 and 30 micrograms/kg BW led to a distinct discharge of GnRH accompanied by emesis or other behaviors suggestive of nausea. Lower doses of CCK (1 and 3 micrograms/kg BW) failed to significantly perturb GnRH release or cause emesis, although NMDA (5 mg/kg BW; racemic form) injected i.v. 3 h after the CCK challenge led to a robust rise in GnRH. In a parallel study, three repetitive i.v. CCK injections at 2h intervals maintained intermittent GnRH release. Pretreatment with a long-acting GnRH receptor antagonist ([AcD2Nal1,4ClPhe2,DTrp3,DArg6,DAla10]GnRH -HOAc) abolished the LH response to CCK, confirming that the action of this peptide was mediated by GnRH release. Although a direct hypothalamic site of action for these agents remains the most likely possibility, since both NMDA and CCK receptors are present in the infundibular region, the present data are consistent with the notion that CCK and, by inference, NMDA may activate GnRH release in part via the stimulation of brainstem emetic centers. Plasma GH, PRL, and cortisol concentrations were also monitored during the course of some of these experiments, and the release of these hormones was observed after the administration of either the 10 or 30 micrograms/kg BW dose of CCK.
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PMID:Cholecystokinin stimulates gonadotropin-releasing hormone release in the monkey (Macaca mulatta). 846 72

From 1990 through 1993, we treated 36 patients with recurrent typical biliary colic but who showed no ultrasonic evidence of cholelithiasis by laparoscopic cholecystectomy. Associated symptoms included nausea (75%), bloating (56%), fatty-food intolerance (53%), vomiting (17%), weight loss (31%), bowel irregularity (28%), reflux or dyspepsia (25%), and fever (17%). Diagnostic evaluation included ultrasound (100%), upper gastrointestinal series (36%), oral cholecystogram (14%), computed tomographic scan (39%), endoscopic retrograde cholangiopancreatography (17%), upper gastrointestinal endoscopy (14%), and hepatobiliary scan (92%). Quantitative hepatobiliary scans in 33 patients revealed a low gallbladder ejection fraction (EF) of less than 35% in 29 patients (88%; mean EF = 9%), and 13 patients experienced reproducible pain after cholecystokinin provocation. All patients underwent attempted laparoscopic cholecystectomy; one case of unsuspected acute acalculous cholecystitis was converted to open laparotomy because of unclear anatomy. Gross and histological examination of the gallbladders revealed chronic inflammation (83%), cholesterolosis (31%), cholesterol crystals or small stones (17%), acute inflammation (8%), polyps (6%), and normal histology (6%); however, blind retrospective scoring of gallbladders revealed significant chronic inflammation in only 38%. In the 2 to 40 months (mean, 14 months) since operation, there have been no deaths (97% follow-up). Laparoscopic cholecystectomy relieved pain in 93% of patients with a low preoperative EF compared with 75% of patients with a normal EF (nonsignificant p value). Persistent abdominal or gastrointestinal complaints included flatulence (31%), loose stools or fecal urgency (29%), belching (29%), indigestion (20%), nausea (11%), and "typical" gallbladder pain (9%). We conclude that many patients with symptoms of biliary colic and scintigraphic evidence of biliary dyskinesia have histologic findings of chronic cholecystitis. Although laparoscopic cholecystectomy usually eliminates biliary colic, persistent nonbiliary complaints are frequent.
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PMID:Chronic acalculous cholecystitis: laparoscopic treatment. 868 Jun 33

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.
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PMID:Food for thought: a critique on the hypothesis that endogenous cholecystokinin acts as a physiological satiety factor. 967 Feb 15


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