Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possibility of malabsorption of triglycerides contained in the diets of children with cholestasis suggests a deficiency of essential fatty acids and, therefore, probable effects on eicosanoid metabolism. Children with either biliary atresia (BA) or syndromatic paucity of interlobular bile ducts (PILBD) were evaluated as to plasma and platelet total lipid fatty acid composition and synthesis of prostaglandins (PG) E1, PGE2, PGI2, PGF2, and thromboxane (TXB2) by whole blood incubated at 37 degrees C for 10 min. In both diseases linoleate deficiency was present as shown by low 18:2 fatty acids in plasma lipids. The children with BA had lower plasma arachidonate than controls but normal eicosanoid synthesis except for excess PGI2. Those with PILBD had low platelet arachidonate and were severely deficient in TXB2 synthesis (less than 10% of controls). Three children with PILBD were fed a supplement of structured triglyceride (Captex 810) intended to provide as much as 10% of energy as linoleate for 2-3 months. Results for these three cases suggested that insufficient linoleate was absorbed to increase plasma linoleate and differences in eicosanoids could not be attributed to linoleate supplementation.
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PMID:Eicosanoid synthesis in children with cholestatic disease. 211 52

Piglet cryptosporidiosis is characterized by intestinal villous damage and malabsorption and by reduced NaCl absorption in response to prostaglandin (PG) release from inflamed tissue. We hypothesized that the PG effect is mediated by the enteric nervous system. Piglets were infected with cryptosporidium and ileal mucosa was studied in Ussing chambers. Studies with tetrodotoxin and indomethacin showed that 75% of the PG-induced alteration in NaCl transport was mediated by the enteric nervous system. Prostacyclin was elevated in infected tissue, and its analog, carbacyclin, mimicked the altered transport response in indomethacin-treated tissue. This carbacyclin response was abolished by tetrodotoxin. The vasoactive intestinal peptide (VIP) receptor antagonist, VIP-10-28, and the muscarinic antagonist, atropine, individually reduced and together abolished the response to carbacyclin, whereas the nicotinic blocker, hexamethonium, reduced the carbacyclin response by 75%. The somatostatin analog, octreotide, and the a-2 adrenergic agonist, clonidine, each abolished the carbacyclin response and partially or completely rectified the altered NaCl transport of the infection. These results indicate that PGs alter NaCl transport in this infection primarily by stimulating cholinergic interneurons that innervate VIPergic and cholinergic motor nerves. The enteric nervous system may be a potential target for pharmacological control of the acute diarrhea in this infection.
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PMID:Role of the enteric nervous system in piglet cryptosporidiosis. 896 31

Piglet cryptosporidiosis is characterized by intestinal villous damage and malabsorption, and by reduced NaCl absorption in response to prostaglandins (PGs), which act directly on the epithelium and indirectly through enteric nerves. We hypothesized that phagocyte-derived reactive oxygen metabolite (ROM) production contributed to PG synthesis and altered transport in inflamed ileum. Ileal mucosa from control and infected piglets was analyzed for villous height, PGE2, catalase (an endogenous antioxidant), and malondialdehyde (MDA, a by-product of lipid peroxidation) from d 2-8 after infection. The response of control ileal mucosa to exogenous ROM and infected mucosa to antioxidant treatment was also studied in tissues mounted in Ussing chambers. Increased levels of MDA on d 2 preceded increased PGE2 on d 3-4, which correlated with the acute diarrheal phase; however the most severe villous atrophy (d 8) correlated with the highest levels of catalase and MDA but low levels of PGE2. Control mucosa responded to H2O2 with indomethacin- and tetrodotoxin-sensitive transient increases in short circuit current (Isc), which were accompanied by increased tissue production of 6-keto-PGF1a, the stable metabolite of PGI2; however, no increased PGE2 production was detectable. A stable analog of PGI2, carbacyclin, mimicked the transient Isc response to H2O2; however, several antioxidants failed to alter the abnormal Isc of infected tissue. These results suggest that there is evidence of increased ROM production in cryptosporidial infection and that intestinal PG synthesis and inhibited NaCl absorption may be mediated partially by ROM in this model. Additional, cooperative factors, such as PGE2 production, however, are likely needed to induce the alterations in ion transport seen in this infection.
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PMID:Reactive oxygen metabolites in piglet cryptosporidiosis. 909 54

Methotrexate (MTX) treatment causes the damage of the small intestine, resulting in malabsorption. The aim of this study was to investigate the effect of prostaglandins (PGs), prostaglandin E1 (PGE1) and prostaglandin I2 (PGI2) analogues, on the MTX-induced damage of rat small intestine by examining the permeability of the small intestinal epithelium. The rats were treated as follows: MTX (15 mg/kg/day), MTX and PGE1/PGI2 analogues (0.5 and 5 micrograms/kg/twice a day), PGE1/PGI2 analogues alone, and sterile saline (control). All drugs were given orally for 5 days. The intestinal permeability of fluorescein isothiocyanate labeled dextran with average molecular mass 4.4 KDa (FD-4) was examined to evaluate the dysfunction of the small intestine by the in vitro everted small intestine technique. The permeation clearance of FD-4 obtained from the in vitro experiment of the MTX-treated rats increased remarkably, but that of the MTX and PGE1/PGI2 analogue-treated rats was significantly lower than that of the MTX-treated rats. These results indicated that PGE1 or PGI2 analogues possibly alleviated the MTX-induced damage of the small intestine of rats.
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PMID:Protective effect of prostaglandins on the methotrexate induced damage of small intestine in rats. 1090 81