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

Following a single, oral dose of Bacillus cereus (2 X 10(8) bacteria) in vitro intestinal absorption of D-glucose, D-galactose, L-arginine, L-histidine, L-ornithine and L-proline in young mice (aged 2--3 1/2 months) decreased. Malabsorption of D-glucose was dose- and time-dependent. Impaired absorption of D-glucose occurred throughtout the length of the small intestine, particularly distally. Following hydrolysis of D-maltose at the brush border, D-glucose absorption in infected mice and that of the untreated controls was similar. Using D-glucose, fluid transfer in the infected intestine and that of the controls was alike. Although slightly lower, fluid transfer in the infected intestine using the other solutes was not significantly different compared with the controls. Glucose-dependent and glucose-independent intestinal fluid transfer in infected animals was like that of the controls. Using old infected mice (aged 8--9 months) intestinal absorption of D-glucose and L-histidine was unchanged compared with young mice. The fresh small intestinal weight in infected mice and the controls was alike. Changes in the histology of the small intestine in young infected mice were small and inconsistent.
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PMID:Bacillus cereus-induced malabsorption in young mice. 9 13

1. Using mouse everted whole small intestine 7 days after a single dose of Phenoclor DP6 (hexachlorobiphenyl) at 1.0 g kg-1 body wt, absorption of D-glucose decreased significantly, probably owing to toxic traces of pentodicholobenzofuran in the PCB preparation and not its high chlorine content. D-glucose tissue accumulation decreased. The serosal fluid transfer also fell but not the gut fluid uptake. D-glucose absorption and fluid transfer remained unchanged following doses of other Phenoclor and Pyralene (PCB) compounds. 2. Using DP6, malabsorption of D-glucose and impaired serosal fluid transfer were not evident 7 days after a single dose of 0.1, 0.25 and 0.50 g kg-1 body wt. One to 21 days after a single dose (1.0 g kg-1 body wt) of DP6, D-glucose absorption and serosal fluid transfer decreased from 3 to 14 days but thereafter became normal. 3. Although absorption of D-galactose, D-glucose following membrane hydrolysis of D-maltose, and L-arginine, L-histidine, L-ornithine and L-proline decreased slightly 7 days after a single dose of Phenoclor DP6,the results were not significant, nor were changes in fluid transfer. 4. Following Phenoclor DP6-treatment, D-glucose malabsorption was abolished by an exogenous energy supply (D-mannose). DP6 affected intracellular metabolism and not the glucose carrier at the membrane brush border. 5. The body-weights and fresh small intestinal weights of mice treated with different PCBs remained unchanged after seven days. The histology of the small intestine showed minimal changes.
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PMID:Polychlorinated biphenyls (phenoclor and pyralene) and intestinal transport of hexoses and amino acids in mice. 82 75

A 9-year-old girl with hereditary dibasicaminoaciduria has been studied for three years. Initially, clinical features were: growth failure; anorexia and aversion to protein, spontaneous daily protein intake averaging only 10 gm; fasting and postprandial venous hyperammonemia; subnormal plasma concentrations of lysine, arginine, ornithine, and citrulline, with generalized hypermonobasicaminoacidemia; abnormally high renal clearances of lysine, arginine, and ornithine; and intestinal malabsorption of lysine and arginine. Intestinal absorption of citrulline, a precursor of arginine and ornithine, was normal. The patient was observed during four sequential 6-month periods as follows: no treatment (Period I); dietary supplement of arginine and lysine (Period II); dietary supplement of citrulline and lysine (Period III); no treatment (Period IV). During Periods II and III growth rate increased 3- to 4-fold, spontaneous protein intake increased 2- to 3-fold, and abnormalities in blood NH3 and the plasma aminogram were partially corrected. In most respects the citrulline plus lysine supplement was more beneficial than that of arginine plus lysine.
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PMID:Hyperdibasicaminoaciduria, hyperammonemia, and growth retardation: Treatment with arginine, lysine, and citrulline. 118 37

Two brothers with hyperdibasicaminoaciduria and postprandial hyperammonemia showed characteristics of lysinuric protein intolerance. Intravenous alanine load produced hyperammonemia that was aborted by oral supplementation with arginine in one brother but not in the other, although both patients had almost the same intestinal malabsorption of arginine. This occurrence suggests that even a small amount of arginine, when absorbed into the blood, can normalize the affected ammonia metabolism of lysinuric protein intolerance. Two patients with cystinuria developed marked hyperammonemia when they received an intravenous alanine load after a 19-hour fast. As both patients displayed a reduced plasma concentration of arginine and ornithine at this time, the hyperammonemia was assumed to arise from the low plasma amino acid level. It seems likely that a decrease in plasma levels of urea cycle substrate causes a failure of the tissue urea cycle metabolism. Thus the impaired ammonia metabolism in lysinuric protein intolerance would be attributed to the low plasma arginine and ornithine levels.
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PMID:Hyperammonemia in lysinuric protein intolerance. 642 86

Blood samples were taken from six overweight women after an overnight fast on three different occasions, before an jejunoileal bypass operation and 1 and 6 months after the operation. The preoperative levels of several plasma free amino acids were significantly elevated, e.g. leucine, isoleucine, valine, lysine, phenylalanine, tyrosine, proline and glutamic acid. One month after the operation all indispensable plasma amino acid concentrations had fallen, in particular the levels of the branched-chain amino acids (BCAA), lysine and tryptophan. Among the dispensable amino acids, plasma tyrosine, arginine and ornithine concentrations were significantly reduced. No further changes of significance were observed in samples taken 5 months later. A close correlation was observed between the plasma levels of retinol-binding protein (RBP) and thyroxine-binding prealbumin (TBPA). One month after the operation the levels of RBP and TBPA had fallen slightly in two subjects and substantially in one subject. A test diet, containing crystalline amino acids, glucose and fat emulsion was given before operation and twice after the operation. Plasma amino acid changes were studied for a period of 2 hours after the meal. The increases in plasma levels following the test meal were lower for many amino acids after the operation. A linear correlation was found between the postprandial increases in BCAA concentrations and the levels of RBP and TBPA. By using complete, carefully defined diets in loading tests, it should be possible to screen for glucose tolerance and amino acid and lipid malabsorption.
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PMID:An oral amino acid loading test before and after intestinal bypass operation for morbid obesity. 713 14

Pyridoxal phosphate is the cofactor for over 100 enzyme-catalysed reactions in the body, including many involved in the synthesis or catabolism of neurotransmitters. Inadequate levels of pyridoxal phosphate in the brain cause neurological dysfunction, particularly epilepsy. There are several different mechanisms that lead to an increased requirement for pyridoxine and/or pyridoxal phosphate. These include: (i) inborn errors affecting the pathways of B(6) vitamer metabolism; (ii) inborn errors that lead to accumulation of small molecules that react with pyridoxal phosphate and inactivate it; (iii) drugs that react with pyridoxal phosphate; (iv) coeliac disease, which is thought to lead to malabsorption of B(6) vitamers; (v) renal dialysis, which leads to increased losses of B(6) vitamers from the circulation; (vi) drugs that affect the metabolism of B(6) vitamers; and (vii) inborn errors affecting specific pyridoxal phosphate-dependent enzymes. The last show a very variable degree of pyridoxine responsiveness, from 90% in X-linked sideroblastic anaemia (delta-aminolevulinate synthase deficiency) through 50% in homocystinuria (cystathionine beta-synthase deficiency) to 5% in ornithinaemia with gyrate atrophy (ornithine delta-aminotransferase deficiency). The possible role of pyridoxal phosphate as a chaperone during folding of nascent enzymes is discussed. High-dose pyridoxine or pyridoxal phosphate may have deleterious side-effects (particularly peripheral neuropathy with pyridoxine) and this must be considered in treatment regimes. None the less, in some patients, particularly infants with intractable epilepsy, treatment with pyridoxine or pyridoxal phosphate can be life-saving, and in other infants with inborn errors of metabolism B(6) treatment can be extremely beneficial.
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PMID:B6-responsive disorders: a model of vitamin dependency. 1676 94

Environmental enteric dysfunction, an asymptomatic condition characterized by inflammation of the small bowel mucosa, villous atrophy, malabsorption, and increased intestinal permeability, is a major contributor to childhood stunting in low-income countries. Here we report the relationship of increased intestinal permeability with serum metabolites in 315 children without acute malnutrition, aged 12-59 months, in rural Malawi. Increased gut permeability was associated with significant differences in circulating metabolites that included lower serum phosphatidylcholines, sphingomyelins, tryptophan, ornithine, and citrulline, and elevated serum glutamate, taurine, and serotonin. Our findings suggest that environmental enteric dysfunction is characterized by alterations in important metabolites involved in growth and differentiation and gut function and integrity.
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PMID:Metabolic alterations in children with environmental enteric dysfunction. 2729 88