Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003123 (anorexia)
 13,794 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Iproniazid was found to reduce food consumption in fasting rats. Combined treatment of iproniazid with tryptophan resulted in a significantly greater anorexic action whilst tryptophan alone had no effect on food consumption. Iproniazid treatment was associated with a significant increase in brain 5-hydroxytryptamine (5-HT) concentration but in association with tryptophan higher brain 5-HT concentrations were recorded. The anorexic action of the iproniazid-tryptophan combination was antagonized in a dose-dependent fashion by methysergide. Equivalent levels of anorexia induced by fenfluramine and mazindol were similarly antagonized by methysergide in a dose-related manner. The results suggest a common role of 5-HT in the inhibition of eating behaviour in fasting rats when anorexia is induced by iproniazid, fenfluramine or mazindol, sensitive to a specific 5-HT antagonist.
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PMID:Inhibition of drug-induced anorexia in rats by methysergide. 0 58

The cause of anorexia associated with neoplasia is unknown, and some investigators have suggested a central mechanism. Recent neurophysiologic studies have revealed the possible role of serotoninergic system involving tryptophan (TRP) and its indole neurotransmitter metabolites in regulating particular aspects of feeding behavior. We therefore studied plasma and brain factors affecting TRP transport through the blood-brain barrier (plasma free and total TRP, albumin, nonesterified fatty acids, plasma neutral amino acids, brain uptake index [BUI] for TRP) and central serotonin metabolism (5-HT, 5-HIAA) in young, anorexic rats bearing the Walker-256 tumor injected intramuscularly. Plasma free TRP, but not plasma total TRP, and, more important, brain TRP and brain 5-HIAA were significantly higher in tumor-bearing rats than in pair-fed control animals. The results suggest an association between altered brain TRP metabolism and feeding behavior in tumor-related anorexia.
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PMID:Brain tryptophan and the neoplastic anorexia-cachexia syndrome. 28 32

The effects of fenfluramine and other sanorectic drugs on the consumption of both protein and total calories by rats given simultaneous access to two isocaloric diets containing 5 or 45 percent casein were examined. Anorectic doses of fenfluramine failed to decrease protein intake but increased the proportion of total dietary calories represented by protein. In contrast, anorectic doses of d-amphetamine decreased protein and calorie consumption proportionately. Subanorectic doses of fenfluramine also increased the proportion of caloric intake represented by protein among animals given prior treatment with the serotonin precursor tryptophan. Fluoxetine, a drug that blocks reuptake of serotonin, similarly spared protein consumption while reducing caloric intake. These observations indicate that two distinct brain mechanisms, sensitive to different drugs, underlie the elective consumption of protein and calories.
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PMID:Fenfluramine and fluoxetine spare protein consumption while suppressing caloric intake by rats. 92 95

The behaviour of some urinary metabolites of tryptophan/nicotinic acid pathway was studied in 7 patients with Parkinson's disease during a 24-day period of levodopa treatment. Corresponding to the appearance of side-effects (agitation, anorexia, dysphagia, glossitis, abdominal pains) in 5 patients there was an increase in urinary Ky, AA, AAG, o-AHA, and 3-HK, while 3-HAA excretion fell. Since no other drugs were given, it was presumed that this effect was due to levodopa administration.
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PMID:Tryptophan/nicotinic acid pathway during levodopa treatment of Parkinsonism. 124 93

Injection of amylin (diabetes-associated peptide) into the hypothalamus induces anorexia, increases brain metabolism of dopamine and serotonin and elevates brain level of tryptophan. When male Sprague-Dawley rats were treated with 50 mg/kg L-tryptophan and L-tyrosine ethyl ester 30 min prior to the intrahypothalamic injection of 2 micrograms amylin, brain tryptophan and tyrosine levels were selectively increased as compared to rats treated with amylin alone. Hypothalamic and striatal serotonin metabolism also appeared to be increased following the amino acid-amylin treatment combination. These results suggest that amylin may increase transport of tyrosine and tryptophan into the brain, and that the increased availability of tryptophan may contribute to increased serotonin turnover observed following intrahypothalamic amylin treatment.
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PMID:Amylin increases transport of tyrosine and tryptophan into the brain. 128 Oct 37

Tumor growth is accompanied by an anorexia mediated by humoral factors that appear to influence appetitive mechanisms in the brain. Because tumor resection is followed by resumption of normal food intake, the circulating anorexigenic substance(s) are produced either by the neoplastic tissue or by the host in response to the tumor. Increased levels of plasma free tryptophan and plasma ammonia have been proposed to mediate cancer anorexia. With animal models, it is often difficult to ascertain whether changes in food intake depend upon metabolic changes or the progressively increasing tumor mass per se. The feeding patterns and biochemical changes that occur during tumor growth were evaluated in 96 male Fischer rats that were inoculated with 10(6) methylcholanthrene sarcoma cells or saline (controls). Rats were placed into metabolic cages equipped with an Automated Computerized Rat Eater Meter to continuously determine meal size and meal number. Plasma free tryptophan and ammonia were evaluated 6, 10, 16, 18, 22, and 26 days after tumor inoculation. Anorexia developed by day 17-18, when food intake started to decrease via a decrease in meal size but not meal number and reached 60% of control by day 26. However, long before anorexia developed, free tryptophan was significantly higher 6 days after tumor inoculation, and the greatest increase occurred after 18 days. Ammonia did not differ from control at any time. Data confirm tumor-associated increases in plasma free tryptophan that occurred before the manifestation of anorexia and support a possible role of brain serotonin in cancer anorexia.
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PMID:The early cancer anorexia paradigm: changes in plasma free tryptophan and feeding indexes. 128 25

Recent concepts in the etiology of Fusarium trichothecene mycotoxicoses have been reviewed. The effect of orally administered trichothecenes on tissue metabolism has been traced from the gastrointestinal tract to the liver and subsequently to blood. It is proposed that the hyperaminoacidemia resulting from trichothecene toxicoses contributes to the behavioral changes observed, including loss of appetite and vomiting. Studies with several species and several trichothecenes have shown that elevated brain tryptophan arising from trichothecene-induced aminoacidemia can subsequently alter regional brain serotonin concentrations. This may produce behaviors such as loss of appetite and muscle incoordination characteristic of the firing of serotonergic neurons. Support is also presented for the concept that other Fusarium metabolites such as fusaric acid may act synergistically with trichothecenes to produce these effects.
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PMID:Recent advances in the understanding of Fusarium trichothecene mycotoxicoses. 147 35

Consistent anorexia was first observed 33 days after inoculating Fischer 344 rats with methylcholanthrene-induced sarcoma. Daily treatment of a similar group of rats with the glutamine synthetase inhibitor, methionine sulfoximine, elicited significant reductions of feeding by day 29 at a dose that had no effect on nontumor-bearing rats. Blood concentrations of ammonia were elevated in both groups of tumor-bearing rats and brain ammonia level was increased in the methionine sulfoximine-treated tumor-bearing rats. Forebrain concentrations of tyrosine, tryptophan, DOPAC and 5-HIAA were elevated in both groups of tumor-bearing rats. Since ammonia is detoxified through the glutamine synthetase reaction, these results suggest that blood and brain ammonia concentrations are more important than the neurochemical consequences of ammonia detoxification for the etiology of cancer anorexia.
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PMID:Methionine sulfoximine intensifies cancer anorexia. 168 54

Inoculation of Buffalo rats with Morris hepatoma produced significant anorexia within four weeks and reduced body weight within two weeks. Blood ammonia concentration was increased by 113% when the rats were euthanized, five days after the development of anorexia. Infusing ammonium salts into normal Buffalo rats also induced anorexia at a blood ammonia concentration comparable to that observed in the tumor-bearing rats. Although ammonia-infused rats exhibited expected increases in brain tyrosine, tryptophan, and metabolites of dopamine and serotonin, these alterations were attenuated in the tumor-bearing rats. These results indicate that hyperammonemia may be a general consequence of experimental cancer and that the increase in ammonia concentration may be of primary importance in the development of experimental cancer-induced anorexia. The rather small alterations in neurotransmitter metabolism in anorectic tumor-bearing rats deemphasize the role aberrations in DA and 5-HT systems in the development of experimental cancer anorexia.
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PMID:Hyperammonemia and anorexia in Morris hepatoma-bearing rats. 168 54

Changes in brain serotonin and tryptophan concentrations probably represent one of the most important mechanisms in the regulation of eating behavior both in experimental animals and in humans. Anorexia, which accompanies numerous diseases, e.g., cancer, liver cirrhosis, and uremia, may recognize an increased brain availability of tryptophan as a common pathogenic mechanism. This will lead to a rise in brain serotonin synthesis, which, in turn, is responsible for a reduction in food intake. According to this hypothesis, the anorexia observed in various diseases could be improved either by a decrease in the cerebral synthesis of serotonin or by a reduction in the entry of tryptophan into the brain.
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PMID:Increased availability of tryptophan in brain as common pathogenic mechanism for anorexia associated with different diseases. 180 75


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