Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of encouraging to ingestive behavior was examined in cats pretreated with amphetamine (AMPH) in a dose sufficient for evoking anorexia (2 mg/kg). AMPH evoked complete refusing of spontaneous food ingestion in all animals. However, the cats could eat in even frantic manner when they were encouraged to ingestive behavior by moving the bowl with food around the place where the animal was sitting in the experimental cage. This result reveals that so called "anorexic syndrome" does not consist simply in a loss of appetite. It may be temporarily suppressed by some additional external stimuli which enable to channel the animal's behavior to the ingestive one.
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PMID:Amphetamine anorexia in cats: the effect of encouraging to ingestive behavior. 387 Jan 52

Rats were exposed to various concentrations of t-butanol as their only available fluid in either the home cage or a schedule-induced drinking situation previously shown to induce overdrinking of ethanol. When animals consumed at least 3 g/kg/day of t-butanol for 90 days, independent of conditions, withdrawal symptoms were observed. This daily intake occurred only when the concentration of t-butanol was 3% (v/v) or greater. The schedule-induction procedure did not induce t-butanol overdrinking at any concentration tested as it does with ethanol, but its use did result in increased probability of the occurrence of withdrawal symptoms over the home cage condition. In no cases was the severity of withdrawal from t-butanol as great as previously reported for ethanol. When the concentration of t-butanol was increased to 3.5% (v/v), severe toxic reactions were found, that included anorexia, self-mutilation, and deaths from no specific determinable causes.
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PMID:Development of physical dependence on t-butanol in rats: an examination using schedule-induced drinking. 719 78

Clinical signs consistent with hepatic lipidosis occurred in six obese adult laboratory cats, housed in a group cage, 6 to 7 weeks after changing their diet from a commercial to a purified diet. The affected cats lost 30 to 40% of their body weight in this time period. This rate of weight loss is compatible with little or no food intake. For treatment, 5 cats were tube-fed three or four times daily with a high-fat liquid diet supplemented with L-citrulline and choline. All cats tolerated the diet, which contained 35% protein on an energy basis. Substantial voluntary food intake resumed 12 to 16 days after initiating treatment. The sixth cat was euthanatized. These observations suggest that 6 to 7 weeks of anorexia, associated with 30 to 40% weight loss, can induce hepatic lipidosis in obese but otherwise healthy cats, and confirm that with appropriate management the prognosis for cats with hepatic lipidosis is favorable.
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PMID:Spontaneous occurrence of hepatic lipidosis in a group of laboratory cats. 833 15

Interleukin-1 (IL-1) induces anorexia via direct action in the brain, and its participation in the pathogenesis of cancer-associated anorexia has been hypothesized. Because the functional ablation of the ventromedial nucleus of hypothalamus (VMH), where IL-1 receptors have been detected, reverses cancer-associated anorexia in tumor-bearing (TB) rats, we hypothesize that cancer anorexia involves the direct effect of IL-1 on the VMH. To test this hypothesis, we investigated whether the intra-VMH injection of the IL-1 receptor antagonist (IL-1ra) improves food intake in anorectic TB rats. Sixteen Fischer rats (approximately 300 g/BW) were injected s.c. with 10(6) trypan-blue viable methylcholanthrene sarcoma cells, and then individually caged. Chow and water were freely available, and food intake was recorded throughout the study. Normal food intake was measured in 8 more rats, injected s.c. with normal saline. Tumor developed in all rats. When TB rats became anorectic, they were randomly assigned to either treatment or control groups. Using stereotaxic techniques, 25 ng of IL-1ra dissolved in normal saline (TB-IL-1ra; n = 8), or an equal volume of normal saline (TB-NS; n = 8) was injected bilaterally into the VMH. After surgery, rats were caged and changes in food intake recorded. At study's end, rats were sacrificed and brains removed for histological confirmation of injection sites. In the TB-NS group, food intake decreased with the occurrence of anorexia. In contrast, the intra-VMH injection of IL-1ra reduced the severity of cancer anorexia, significantly improving food intake in TB-IL-1ra rats. Data indicate that centrally acting IL-1 plays a significant role in the development of cancer anorexia.
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PMID:Relationship between interleukin-1 and cancer anorexia. 874 51

During tumor growth, anorexia and reduced food intake markedly contribute to the development of malnutrition, thus worsening overall patients' survival. A better understanding of the pathophysiology of eating behavior may lead to new and more effective therapies, aiming at counteracting the detrimental effects of anorexia and reduced food intake on nutritional status and survival in cancer patients. Brain tryptophan and serotonin concentrations seem to play a pivotal role in the regulation of eating behavior. Increased brain serotonin activity is indeed associated with a reduction of food intake. It has been recently hypothesized that increased availability of tryptophan to the brain and the consequent increased serotonin activity may represent the pathogenic mechanism for cancer-associated anorexia. According to this hypothesis, the modulation of brain serotonin activity may result in an improvement of anorexia. Reducing brain tryptophan availability represents a possible mechanism to restore brain serotonin activity to normal. There is evidence that the oral administration of neutral amino acids competing with tryptophan for brain entry results in a significant improvement of cancer anorexia. The same treatment may also be effective in improving secondary anorexia, which is associated with other chronic illnesses, including renal and liver failure, sepsis, and so forth, sharing a similar pathogenic mechanism.
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PMID:Cancer anorexia: new pathogenic and therapeutic insights. 885 Feb 21

Cancer is consistently associated with anorexia. The Lobund-Wistar rat model of prostate cancer exhibits clinical manifestations (including anorexia) that resemble many aspects of the human disease. Cytokines are proposed to be involved in cancer-associated anorexia. Here we investigated mRNA profiles of feeding-modulatory cytokines and neuropeptides in specific brain regions of anorectic Lobund-Wistar rats bearing prostate adenocarcinoma tumor cells. Interleukin (IL)-1beta system components (ligand, signaling receptor, receptor accessory proteins, receptor antagonist), tumor necrosis factor-alpha, transforming growth factor-beta1, glycoprotein 130 (IL-6 receptor signal transducer), proopiomelanocortin (POMC, opioid peptide precursor), and neuropeptide Y (NPY) mRNAs were analyzed with sensitive and specific RNase protection assays. The same brain region sample was assayed for all components. The data show that early anorexia in tumor-bearing rats was associated with an upregulation of IL-1beta mRNA in the brain regions examined (cerebellum, cortex, and hypothalamus). IL-1 receptor antagonist (IL-1Ra) mRNA and IL-1 receptor type I mRNA levels were also significantly increased in the cortex and hypothalamus. All other cytokine components, POMC, or NPY mRNA levels were not significantly different between tumor-bearing and pair-fed (control) rats. IL-1beta mRNA and IL-1Ra mRNA were also significantly upregulated in the spleen of tumor-bearing rats. These data suggest that 1) IL-1beta mRNA upregulation in the brain may be relevant to the anorexia exhibited by the tumor-bearing Lobund-Wistar rat and 2) in vivo characterization of cytokine components in discrete brain regions during cancer is necessary to understand underlying molecular mechanisms responsible for cancer-associated neurological manifestations.
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PMID:Brain cytokine mRNAs in anorectic rats bearing prostate adenocarcinoma tumor cells. 968 94

The activity anorexia syndrome is characterized by reduced food intake and body weight compared to control levels and increasing levels of physical activity. To induce it, food-restricted rats are confined in running wheels except during the daily meal. We tested whether activity in a flat circular alley also produces the activity anorexia syndrome. In Experiment 1, food-restricted rats were maintained in alleys, wheels, or home cages (control condition). In Experiment 2, they were maintained in alleys, wheels, novel cages, or home cages. The novel cage was added to control for the possibility that the alley might produce an anorectic effect simply because it was a new living space. The alley did not produce the activity anorexia syndrome whereas the wheel did. Although weight loss was greater in the alley than home-cage condition, the alley produced weak, inconsistent suppression of feeding. Moreover, the suppression produced by the alley may have stemmed simply from living in a novel environment. Finally, in contrast to wheel running, alley activity decreased over days. Alley activity, unlike wheel running, may not be reinforcing. Likely, a physical activity must be reinforcing to produce the activity anorexia syndrome. Implications for anorexia nervosa were discussed.
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PMID:Activity in the circular alley does not produce the activity anorexia syndrome in rats. 1074 4

To compare a novel controlled-release formulation of metoclopramide with placebo in patients with cancer-associated dyspepsia syndrome, 26 adult patients with a >/=1 month history of cancer-associated dyspepsia syndrome were randomized to receive either controlled-release metoclopramide 40 mg every 12 hours or matching placebo for a period of 4 days. On day 5, patients crossed over to the alternate treatment for a further period of 4 days. Dose adjustments and rescue antiemetics were permitted during both phases. Nausea, anorexia, bloating, vomiting/retching, and drowsiness were assessed on a 100-mm VAS scale in a daily diary. On the last day of treatment of each phase, nausea was significantly lower in the controlled-release metoclopramide group compared to placebo (17 +/- 12 mm versus 12 +/- 10 mm). Nausea scores tended to increase across days during the placebo phase and to decrease during the controlled-release metoclopramide phase. There was a trend for improvement in the intensity of all symptoms on controlled-release metoclopramide with the exception of appetite, but this trend only reached statistical significance for nausea. The frequency and severity of elicited adverse events did not differ significantly between treatments, although drowsiness, dizziness, and poor sleep were somewhat higher in the placebo group. In no case was it necessary to discontinue controlled-release metoclopramide because of toxicity. These results indicate that controlled-release metoclopramide reduces gastrointestinal symptoms in this population of advanced cancer patients.
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PMID:A double-blind, crossover study of controlled-release metoclopramide and placebo for the chronic nausea and dyspepsia of advanced cancer. 1090 23

Cancer is frequently associated with anorexia, weight loss, negative nitrogen balance, and skeletal-muscle wasting. Depletion of skeletal-muscle mass is critical to overall survival of the patient, can prolong rehabilitation to normal function after recovery, and decreases quality of life in a palliative-care setting. The biochemical and physiologic bases of cancer-associated muscle wasting have been most fully investigated in animal models. These studies provide evidence for suppressed protein synthesis and activated proteolysis in cancer-associated muscle wasting and indicate a need for both anabolic and anticatabolic therapies. Several humoral factors of host or tumor origin are implicated in altered muscle-protein metabolism, including cytokines, metabolites of arachidonic acid, and a proteolysis-inducing glycoprotein; their interrelationships are less well characterized. Several catabolic mediators may share common downstream mechanisms because they ultimately activate the ATP-, ubiquitin-, and proteasome-dependent intracellular proteolytic system. Although important gaps in our current understanding remain, data available from animal studies can be used as a basis to develop relevant studies in human subjects.
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PMID:Regulation of skeletal-muscle-protein turnover in cancer-associated cachexia. 1105 10

A three-year old male cynomolgus macaque (Macaca fascicularis) presented with clinical signs of anorexia and depression that decreased over a 48-hour period. Results of abdominal radiography abdominocentesis, blood biochemical analysis and CBC suggested septic peritonitis. Exploratory laparotomy revealed multiple perforations along the mesenteric border of the small intestine. Necropsy revealed masses of fibrous material in the stomach and cecum. Multiple mucosal ulcerations, as well as linear fibrous material, were found in the small intestine. The ulceration, perforations, and septic peritonitis were attributed to the ingestion of rope that had been attached to the animal's cage as an environmental-enrichment device.
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PMID:Environmental enrichment-related injury in a macaque (Macaca fascicularis): intestinal linear foreign body. 1109 42


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