Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.1.17 (ornithine decarboxylase)
 6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The evidence for an enteropancreatic trophic axis is reviewed. Luminal nutrition is essential for the maintenance of normal intestinal mucosal, as well as exocrine pancreatic structure and function. Exclusion of luminal nutrition leads to mucosal hypoplasia and hypofunction with similar changes in the pancreas. The trophic effect of luminal nutrition may be mediated through the release of regulatory peptides with endocrine or paracrine effects. Enteroglucagon is the strongest candidate for the role of "enterotrophin" while cholecystokinin (CCK) markedly influences pancreatic growth. Thus, CCK not only stimulates exocrine pancreatic secretion but makes acinar cells divide and the pancreas grow. The cellular mechanisms whereby trophic peptides influence normal and adaptive growth are also discussed with emphasis on polyamines (putrescine, spermidine and spermine) and the key enzymes controlling their synthesis (ornithine decarboxylase [ODC]) and degradation (diamine oxidase [DAO]). When polyamine synthesis is blocked with the ODC inhibitor difluoromethyl ornithine (DFMO), the adaptive intestinal hyperplasia of pancreaticobiliary diversion is either inhibited or completely prevented. A proposed sequence of events might be: luminal nutrients, particularly long chain fat, reach the ileum and colon and stimulate increased enteroglucagon release. Enteroglucagon binds to cell receptors and triggers an intracellular cascade involving ODC and the polyamines which, in turn, stimulate RNA polymerase, DNA, RNA and protein synthesis, cell division and adaptive tissue growth.
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PMID:[Potential adaptation of the gastrointestinal system. Existence of an enteropancreatic trophic axis, the role of hormones and polyamines]. 393 Dec 14

The effects of prostaglandins E1 and E2, indomethacin, arachidonic acid, and 8,11,14-eicosatrienoic acid on the rate of (14C)-acetate incorporation into lipids in mouse mammary gland explants were studied. Prostaglandins E1 and E2, as well as their precursors 8,11,14-eicosatrienoic acid and arachidonic acid, inhibited the rate of (14C)-acetate incorporation into lipids, possibly through increased cAMP levels or through end product inhibition of acetyl CoA carboxylase and fatty acid synthetase by long chain fatty acids. Indomethacin at concentrations of 50 micrograms/ml and above significantly reduced the basal rate of 14C-acetate incorporation into lipids, but it did not abolish the prolactin response. Since the prostaglandins, at low concentrations, have prolactin-like actions on RNA synthesis and ornithine decarboxylase activity, and since indomethacin attenuates the actions of prolactin on RNA synthesis, casein synthesis, and ornithine decarboxylase activity, it seems apparent that all of the metabolic actions of prolactin in the mammary gland may not occur via the same primary mechanism.
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PMID:Effects of prostaglandins on the prolactin stimulation of lipid biosynthesis in mouse mammary gland explants. 657 26

Rats with atrophic intestinal mucosa due to enteral nutrition supplied by an elemental diet (ED) for 4 weeks or more, received a fat-enriched ED containing 10% long chain triglycerides (10% FED) orally. The atrophic ileal mucosa became trophic 4 weeks after administration of the 10% FED. Ornithine decarboxylase activity in the ileal mucosa increased 3 days after the administration of 10% FED. Rats with atrophic intestinal mucosa that had undergone a 70% proximal jejunoileectomy, received an oral ED containing 4% long chain triglycerides (4% FED). In the jejunoileectomized rats, marked proliferation of the remaining ileum was observed irrespective of diet, when compared with the transected control group. In the transected group, the 4% FED had trophic effects on the ileum, but in the jejunoileectomized group, the 4% FED had no significant trophic effect on the remaining ileum. In conclusion, long chain triglycerides had mild trophic effects on ileal mucosa and were effective in the treatment of atrophic intestinal mucosa. However, the trophic effects of fat were apparently masked by the marked proliferation of the ileal mucosa following jejunoileectomy.
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PMID:The trophic effects of long chain triglycerides on the atrophic ileal mucosa of rats. 800 14