Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.13.11.12 (lipoxygenase)
 8,696 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the peripheral prostaglandin synthetizing system may at least partly involved in the anorexia that follows central interleukin-1 beta (IL-1) administration, this study was undertaken to investigate the effect of ibuprofen (ip), selective cyclooxygenase blocker and AA 861, selective lipoxygenase inhibitor, on changes of food and water intake by a single injection of IL-1 (2 micrograms/rat, ip). We demonstrated that food and water intake were suppressed by peripheral administration of IL-1. Throughout the entire observation periods, suppressed food intake was partially restored to control levels by ibuprofen, while water intake completely restored. In addition, no significant differences about water/food intake were observed in the IL-1 + ibuprofen-treated groups, respectively. In the next experiment, IL-1 induced anorexia was also partially restored to the control level following pretreatment with AA 861. These results may suggest that other mechanism including lipoxygenase blocker besides prostaglandin production may be involved in IL-1 induced anorexia.
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PMID:Both cyclooxygenase and lipoxygenase inhibitor partially restore the anorexia by interleukin-1 beta. 140 57

IL-1 and other cytokines mediate several components of both acute and chronic pathological processes observed in patients with cancer and chronic infection. Cachexia ranks as one of the more prominent aspects of several diseases and the present studies demonstrate that recombinant forms of either IL-1 beta or IL-1 alpha reduce food intake in experimental animals. In meal-fed rats, a single injection of IL-1 induces a 40% reduction [table: see text] in food intake, whereas daily injections slow normal weight gain. The anorexic response to IL-1 is prevented by cyclooxygenase inhibitors, although this is unlikely due to a central nervous system effect. Reduced production of cyclooxygenase products such as PGE2 also occurs in rats fed supplemental N-3 fatty acids, and this was associated with a decreased anorexic response to IL-1. Therefore, one mechanism by which IL-1 induces anorexia appears to require cyclooxygenase metabolites, such as PGE2. N-3 fatty acid supplements also reduce the severity of host responses to inflammation and infection. Part of this is due to decreased cyclooxygenase products; however, part also may be due to reduced synthesis of IL-1. Blood leukocytes from human subjects taking oral N-3 supplements produce 60% less IL-1. The ability of N-3 fatty acids to reduce IL-1 synthesis appears to be via the lipoxygenase pathway. Therefore, N-3 fatty acids may be beneficial to patients with anorexia, since such supplements would decrease both the anorexic response to IL-1 via reduced cyclooxygenase metabolites and the production of IL-1, via altered lipoxygenase metabolites.
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PMID:Interleukin-1, anorexia, and dietary fatty acids. 219 79

Sulfasalazine is metabolized by intestinal bacteria, resulting in the release of sulfapyridine and 5-aminosalicylate. The drug is useful in the treatment of active ulcerative colitis as well as in preventing relapses of the disease in remission. Although effective in active Crohn's disease as well, sulfasalazine appears to be of greater benefit to patients with colitis and ileocolitis than those with ileitis alone. 5-Aminosalicylate itself is efficacious when given in enema and suppository form; oral agents capable of delivering 5-aminosalicylate to distal disease sites are now under study. The drug's mechanism of action may relate to its effects on prostaglandin synthesis or interference with arachidonic acid metabolism by the lipoxygenase pathway. Common adverse reactions of sulfasalazine, including nausea, headache, and anorexia, as well as hemolysis, are associated with high serum sulfapyridine levels and often can be avoided by lowering the dose of sulfasalazine. Mild allergic reactions, such as rash and fever, may be overcome by gradual desensitization.
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PMID:Sulfasalazine. Pharmacology, clinical use, toxicity, and related new drug development. 614 10

We measured daily food intake and body weight in rats before and after the induction of colitis by intrarectal administration of either 2,4,6-trinitrobenzenesulfonic acid in ethyl alcohol (TNBE) or 4% acetic acid (AA). Administration of TNBE or AA induced inflammation in the distal colon, which was reflected by a significant increase in myeloperoxidase (MPO) activity in the colon. On days 1, 2, and 3 after induction of colitis by TNBE, food intake fell by 80, 70, and 50%, respectively, compared with pretreatment values; food intake returned to normal by day 4. Body weight fell within 24 h after induction of colitis and remained 10% less than control for at least 5 days. Colitis induced by AA produced a similar pattern and degree of decreased food intake and weight loss. Treatment with the 5'-lipoxygenase inhibitor MK-886 significantly reduced concentrations of leukotriene B4 in the colon of TNBE-treated rats but did not affect food intake. In contrast, the cyclooxygenase inhibitor indomethacin decreased prostaglandin E2 concentrations in the colon but also attenuated the suppression of feeding by 52 and 64% on the first 2 days after induction of colitis by TNBE. These results identify a specific prostaglandin-mediated suppression of feeding in the rat with acute colitis induced by TNBE and illustrate the utility of this model for studying mechanisms underlying anorexia associated with inflammation of the gastrointestinal tract.
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PMID:On the suppression of food intake in experimental models of colitis in the rat. 849 96