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)

Infusions of cholecystokinin (CCK) may exert their effects on appetite by inducing feelings of nausea or anxiety. In this double blind, placebo controlled crossover study, the impact of these effects on appetite were examined. Fifteen male subjects received a 20 min i.v. infusion of cholecystokinin octapeptide (CCK-8) (4 ng/kg/min) or saline. The infusion commenced 20 min after a soup preload and 10 min before an ad libitum test meal. Visual analogue scales of appetite and mood were measured over 3 h, and subjects were instructed to report any other sensations they experienced over this time. CCK-8 significantly reduced premeal hunger, elevated premeal anxiety, and reduced energy intake at the ad libitum test meal. Meal duration and rate of eating (kcal/min) were also significantly reduced after CCK-8. After the smaller meal with CCK-8, hunger rose quickly to a higher level than with placebo. The return of hunger was commensurate with the smaller amount of energy consumed and indicated that CCK did not exert an enduring effect on hunger suppression. A significant correlation was found between the reduction in energy intake and hunger (r = 0.75 p < 0.01), but not with anxiety (r = 0.15 not significant). Analyses were performed separately on subjects who did (n = 8), or did not (n = 7) report gastrointestinal disturbance. Energy intake was reduced by 56.6% and 44.6%, respectively. These results indicate that, although feelings of anxiety and nausea may accompany CCK infusions, they are not necessary for the effects of CCK on appetite. These data provide support for a role of CCK in satiety.
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PMID:Untangling the effects of hunger, anxiety, and nausea on energy intake during intravenous cholecystokinin octapeptide (CCK-8) infusion. 985 80

Both distension of the stomach and activation of small intestinal chemoreceptors by nutrients have been implicated in the induction of postprandial sensations. Studies were performed in healthy human subjects to investigate the roles of gastric distension and activation or inhibition of small intestinal chemoreceptors in the generation of pleasant (fullness) and unpleasant (nausea, pain) gastrointestinal sensations. The proximal stomach was distended by inflating a balloon attached to a gastric tube with air, while the duodenum was perfused with nutrient solutions, either lipid or carbohydrates. In additional experiments, the upper small intestinal mucosa was anaesthetised by topical anaesthesia or an antagonist to cholecystokinin (CCK)-A receptors given intravenously during duodenal lipid infusion. Gastric distension induced sensations of epigastric pressure and pain, while during duodenal infusion of both carbohydrate and lipid, fullness was described as a more meal-like sensation. In addition, lipid but not carbohydrate infusion resulted in significant nausea. The sensory experience evoked by lipid was diminished by both topical mucosal anaesthesia and CCK-A receptor blockade. The data provide evidence for the involvement of small intestinal chemoreceptors in the modulation of sensations induced by gastric distension.
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PMID:Role of intestinal chemoreception in the induction of gastrointestinal sensations. 993 12

The main factors involved in the pathophysiology of fat induced dyspepsia were investigated by reviewing a series of controlled double blind randomised studies which sought to determine the role of nutrient fat and the postprandial release of cholecystokinin (CCK) in the development of dyspeptic symptoms in healthy volunteers and in patients with functional dyspepsia. The studies showed that during distension of the stomach, lipids are a major trigger of dyspeptic symptoms such as nausea, bloating, pain, and fullness, and that they modulate upper gastrointestinal sensations and symptoms in a dose related fashion. CCK is a major mediator of the sensitisation of gastric perception by lipids in patients with functional dyspepsia as the CCK-A receptor antagonist dexloxiglumide markedly diminishes this effect. The studies provide important insights into the mechanisms underlying gastrointestinal perception in response to fat and the role of CCK in patients with functional dyspepsia.
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PMID:The role of fat and cholecystokinin in functional dyspepsia. 1207 66

Family planners responding to an annual oral contraceptives (OC) survey tended to recommend switching pills for complaints of headaches and mood swings and life style changes for the complaint of weight gain. Nearly 3/4 of survey respondents indicated that headaches and mood swings affected less than 5% of their patients. On the other hand, 29% reported that less than 5% of patients complained of weight gain; 27% said 10% complained; 19% said 10-15% complained; 10% said 15 to 20% complained; and 14% said more than 20% of patients complained of weight gain. 57% of the 137 respondents would instruct patients to exercise more and reduce calorie intake, and only 13% would change a patient's pill formulation because of weight gain. Nausea, breast changes, breakthrough bleeding, and compliance issues seem to be more relevant to birth control pills. However, a study indicated that women who discontinue more often do it because more often do it because of weight gain or acne than because of irregular bleeding or amenorrhea. Some women have gained 10-30 lbs using OCs. Researchers in Sweden recorded the secretion of the satiety hormone cholecystokinin during a 24-hour period before and during administration of OCs to 9 women, and found that pills suppressed the serum profiles of cholecystokinin inducing the feeling of hunger. Further studies are needed to evaluate the mechanism of this effect.
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PMID:Lifestyle changes most often suggested for weight complaints. Special report: annual pill survey. 1234 23

The effects of evodiamine on gastric emptying, gastrointestinal transit, and plasma levels of cholecystokinin (CCK) were studied in male rats. Evodiamine, isolated from the dry unripened fruit of Evodia rutaecarpa Bentham (a Chinese medicine named Wu-chu-yu), has been recommended for abdominal pain, acid regurgitation, nausea, diarrhea, and dysmenorrhea. Gastrointestinal motility was assessed in rats 15 min after intragastric instillation of a test meal containing charcoal and Na(2)51CrO(4). Gastric emptying was determined by measuring the amount of radiolabeled chromium contained in the small intestine as a percentage of the initial amount received. Gastrointestinal transit was evaluated by calculating the geometric center of distribution of the radiolabeled marker. Blood samples were collected for CCK radioimmunoassay (RIA). After administration of evodiamine (0.67-6.00 mg/kg), both gastric emptying and gastrointestinal transit were inhibited, whereas the plasma concentration of CCK was increased in a dose-dependent manner. The selective CCK(1) receptor antagonists, devazepide and lorglumide, effectively attenuated the evodiamine-induced inhibition of gastric emptying and gastrointestinal transit. L-365,260 (3R-(+)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4-benzodiazepine-3-yl)-N'-(3-methylphenyl)-urea), a selective CCK(2) receptor antagonist, did not alter the evodiamine-induced inhibition of gastric emptying and gastrointestinal transit. These results suggest that evodiamine inhibits both gastric emptying and gastrointestinal transit in male rats via a mechanism involving CCK release and CCK(1) receptor activation.
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PMID:Effects of evodiamine on gastrointestinal motility in male rats. 1246 63

Patients with biliary dyskinesia have biliary colic, a normal gallbladder ultrasound, and a gallbladder ejection fraction typically less than 35%. We report a retrospective review of 70 patients with biliary dyskinesia who underwent cholecystectomy. Seventy-seven percent of the patients were women. Average age was 40. The most common symptoms were right upper quadrant pain, nausea, vomiting, and fatty food intolerance. All patients underwent a cholecystokinin-hepatobiliary scan or cholecystokinin-oral cholecystogram. Average ejection fractions were 20.2% and 28.4% respectively. Average post-operation follow-up was 10.9 months. Eighty-four percent of patients (59 of 70) reported improvement at follow-up. Eight patients had ejection fractions greater than 35%; seven of them reported improvement after cholecystectomy. Eleven patients did not improve after cholecystectomy; their average ejection fraction was 25%. These patients also had atypical symptoms (mid-epigastric pain and reflux symptoms). We believe cholecystectomy is effective therapy for biliary dyskinesia. Surgical outcomes could be improved by careful histories distinguishing biliary colic from other complaints. Less reliance should be placed on the ejection fraction when the patient has biliary colic without another etiology of abdominal pain.
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PMID:Outcomes of surgical therapy for biliary dyskinesia. 1450 24

The gastrointestinal effects of intraluminal fats may be critically dependent on the chain length of fatty acids released during lipolysis. We postulated that intraduodenal administration of lauric acid (12 carbon atoms; C12) would suppress appetite, modulate antropyloroduodenal pressure waves (PWs), and stimulate the release of cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) more than an identical dose of decanoic acid (10 carbon atoms; C10). Eight healthy males (19-47 yr old) were studied on three occasions in a double-blind, randomized fashion. Appetite perceptions, antropyloroduodenal PWs, and plasma CCK and GLP-1 concentrations were measured during a 90-min intraduodenal infusion of 1) C12, 2) C10, or 3) control (rate: 2 ml/min, 0.375 kcal/min for C12/C10). Energy intake at a buffet meal, immediately after completion of the infusion, was also quantified. C12, but not C10, suppressed appetite perceptions (P < 0.001) and energy intake (control: 4,604 +/- 464 kJ, C10: 4,109 +/- 588 kJ, and C12: 1,747 +/- 632 kJ; P < 0.001, C12 vs. control/C10). C12, but not C10, also induced nausea (P < 0.001). C12 stimulated basal pyloric pressures and isolated pyloric PWs and suppressed antral and duodenal PWs compared with control (P < 0.05 for all). C10 transiently stimulated isolated pyloric PWs (P = 0.001) and had no effect on antral PWs but markedly stimulated duodenal PWs (P = 0.004). C12 and C10 increased plasma CCK (P < 0.001), but the effect of C12 was substantially greater (P = 0.001); C12 stimulated GLP-1 (P < 0.05), whereas C10 did not. In conclusion, there are major differences in the effects of intraduodenal C12 and C10, administered at 0.375 kcal/min, on appetite, energy intake, antropyloroduodenal PWs, and gut hormone release in humans.
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PMID:Effects of intraduodenal fatty acids on appetite, antropyloroduodenal motility, and plasma CCK and GLP-1 in humans vary with their chain length. 1530

We recently reported that intraduodenal infusion of lauric acid (C12) (0.375 kcal/min, 106 mM) stimulates isolated pyloric pressure waves (IPPWs), inhibits antral and duodenal pressure waves (PWs), stimulates release of cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1), and suppresses energy intake and that these effects are much greater than those seen in response to isocaloric decanoic acid (C10) infusion. Administration of C12 was, however, associated with nausea, confounding interpretation of the results. The aim of this study was to evaluate the effects of different intraduodenal doses of C12 on antropyloroduodenal (APD) motility, plasma CCK and GLP-1 concentrations, appetite, and energy intake. Thirteen healthy males were studied on 4 days in double-blind, randomized fashion. APD pressures, plasma CCK and GLP-1 concentrations, and appetite perceptions were measured during 90-min ID infusion of C12 at 0.1 (14 mM), 0.2 (28 mM), or 0.4 (56 mM) kcal/min or saline (control; rate 4 ml/min). Energy intake was determined at a buffet meal immediately following infusion. C12 dose-dependently stimulated IPPWs, decreased antral and duodenal motility, and stimulated secretion of CCK and GLP-1 (r > 0.4, P < 0.05 for all). C12 (0.4 kcal/min) suppressed energy intake compared with control, C12 (0.1 kcal/min), and C12 (0.2 kcal/min) (P < 0.05). These effects were observed in the absence of nausea. In conclusion, intraduodenal C12 dose-dependently modulated APD motility and gastrointestinal hormone release in healthy male subjects, whereas effects on energy intake were only apparent with the highest dose infused (0.4 kcal/min), possibly because only at this dose was modulation of APD motility and gastrointestinal hormone secretion sufficient for a suppressant effect on energy intake.
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PMID:Dose-related effects of lauric acid on antropyloroduodenal motility, gastrointestinal hormone release, appetite, and energy intake in healthy men. 1596 31

Opiates are the primary treatment for pain management in cancer patients reporting moderate to severe pain, and are being increasingly used for non-cancer chronic pain. However, prolonged administration of opiates is associated with significant problems including the development of antinociceptive tolerance, wherein higher doses of the drug are required over time to elicit the same amount of analgesia. High doses of opiates result in serious side effects such as constipation, nausea, vomiting, dizziness, somnolence, and impairment of mental alertness. In addition, sustained exposure to morphine has been shown to result in paradoxical pain in regions unaffected by the initial pain complaint, and which may also result in dose escalation, i.e. 'analgesic tolerance'. A concept that has been gaining considerable experimental validation is that prolonged use of opioids elicits paradoxical, abnormal pain. This enhanced pain state requires additional opioids to maintain a constant level of antinociception, and consequently may be interpreted as antinociceptive tolerance. Many substances have been shown to block or reverse antinociceptive tolerance. A non-inclusive list of examples of substances reported to block or reverse opioid antinociceptive tolerance include: substance P receptor (NK-1) antagonists, calcitonin gene-related peptide (CGRP) receptor antagonists, nitric oxide (NO) synthase inhibitors, calcium channel blockers, cyclooxygenase (COX) inhibitors, protein kinase C inhibitors, competitive and non-competitive antagonists of the NMDA (N-methyl-D-aspartate) receptor, AMPA (alpha-amino-3-hydroxy-5-methyl-4 isoxazolepropionic acid) antagonists, anti-dynorphin antiserum, and cholecystokinin (CCK) receptor antagonists. Without exception, these substances are also antagonists of pain-enhancing agents. Prolonged opiate administration indeed induces upregulation of substance P (SP) and calcitonin gene-related peptide (CGRP) within sensory fibers in vivo, and this is accompanied by an enhanced release of excitatory neurotransmitters and neuropeptides from primary afferent fibers upon stimulation. The enhanced evoked release of neuropeptides is correlated with the onset of abnormal pain states and opioid antinociceptive tolerance. Importantly, the descending pain modulatory pathway from the brainstem rostral ventromedial medulla (RVM) via the dorsolateral funiculus (DLF) is critical for maintaining the changes observed in the spinal cord, abnormal pain states and antinociceptive tolerance, because animals with lesion of the DLF did not show enhanced evoked neuropeptide release, or develop abnormal pain or antinociceptive tolerance upon sustained exposure to opiates. Microinjection of either lidocaine or a CCK antagonist into the RVM blocked both thermal and touch hypersensitivity as well as antinociceptive tolerance. Thus, prolonged opioid exposure enhances a descending pain facilitatory pathway from the RVM that is mediated at least in part by CCK activity and is essential for the maintenance of antinociceptive tolerance.
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PMID:Is paradoxical pain induced by sustained opioid exposure an underlying mechanism of opioid antinociceptive tolerance? 1621 2

Biliary dyskinesia is a potential cause for acalculous biliary colic in pediatric patients. A triad of symptoms and signs, consisting of abdominal pain (with or without associated nausea or fatty food intolerance), absence of gallstones, and an abnormally low cholecystokinin-stimulated gallbladder ejection fraction is used to diagnose the disorder. In several small pediatric case series, cholecystectomy resulted in symptomatic improvement in a majority of patients with biliary dyskinesia. However, the diagnosis of biliary dyskinesia and appropriate management remain controversial. This review discusses the purported pathophysiology of biliary dyskinesia and the data available regarding diagnosis and treatment of this entity in the pediatric population.
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PMID:Biliary dyskinesia in pediatrics. 1653 82


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