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)

The suitability of the simultaneous azocoupling reaction with 1-naphthyl-beta-D-glucoside and hexazonium-p-rosanilin in the detection of the activity of lactase (or lactase-beta-glucosidase complex) in jejunal biopsies of patients with various forms of the malabsorption syndrome was tested. Results were compared with those obtained with the indigogenic method using 4-Cl-5-Br-3-indolyl-beta-D-fucoside which is the method of choice. Both methods gave identical results as far as the relative intensity of the brush border staining was concerned. The azocoupling method applied in unfixed cold microtome sections can be recommended for the routine diagnostics of the malabsorption syndrome when the indolyl substrate is not available.
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PMID:Suitability of the azocoupling reaction with 1-naphthyl-beta-D-glucoside for the histochemical demonstration of lactase (lactase-beta-glucosidase complex) in human enterobiopsies. 5 35

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

We have studied 5 infants with persistent severe diarrhea from birth and marked abnormalities of absorption associated with failure to thrive leading to death in 4 infants. Three had siblings who died and a sibling of a 4th is ill at present, all with a similar illness; 2 were the products of consanguinous marriages. Exhaustive investigation failed to identify a recognized disease entity in any patient. Steatorrhea, sugar malabsorption, dehydration, and acidosis were severe in all patients, whatever the diet fed. Total parenteral nutrition was used, but excessive stool water and electrolyte losses persisted even when nothing was fed by mouth. There was no evidence of a hematological or consistent immunological defect in any infant and no abnormalities of intestinal hormones were noted. In the duodenal mucosa of all infants we saw similar abnormalities characterized by villus atrophy, crypt hypoplasia without an increase in mitoses or inflammatory cell infiltrate in the lamina propria and in villus enterocytes absence of a brush border, increase in lysosome-like inclusions, and autophagocytosis. In 3 infants studied by marker perfusion of the proximal jejunum we found abnormal glucose absorption and a blunted response of Na+ absorption to actively transported nonelectrolytes; in 2 there was net secretion of Na+ and H2O in the basal state. Our patients evidently suffered from a congenital enteropathy which caused profound defects in their capacity to assimilate nutrients. The similar structural lesion seen in the small intestinal epithelium of all of our cases undoubtedly contributed to their compromised intestinal function, but the pathogenesis of this disorder, if indeed it is a single disease, remains obscure.
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PMID:Familial enteropathy: a syndrome of protracted diarrhea from birth, failure to thrive, and hypoplastic villus atrophy. 10 Mar 67

General evidence of malnutrition such as loss in body weight associated with intestinal parasitism has been attributed to decreased food intake, to intestinal malabsorption, and to change in host basal metabolism. To establish the relative importance of these factors in this regard, rats with trichinosis were studied. The weights of infected and uninfected animals were followed after being placed on one of three feeding regimens for 1 week--stock diet ad libitum, intraduodenal nutrition, and intravenous nutrition. Infected rats on a stock diet lost weight whereas those on the other two regimens maintained the same weight pattern as uninfected counterparts. The maintainance of body weight occurred despite alterations at the level of the intestinal brush border as indicated by a depression of intestinal disaccharidase activities (sucrase and lactase) and by reduction of monosaccharide absorption (measured as accumulation of beta-methyl glucoside) in the proximal, heavily infected region of the small intestine. There was no compensatory increase in enzyme activity nor in the absorptive capacity in the distal gut. Results support the conclusion that inadequate oral food intake rather than changes in basal metabolism or intestinal pathophysiology accounts for weight loss during the intestinal phase of infection.
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PMID:Enteral and parenteral feeding to evaluate malabsorption in intestinal parasitism. 11 Jan 62

Histochemical examination of aspiration biopsy specimens of the duodenum in 8 healthy volunteers and 23 patients with various gastrointestinal disorders revealed no characteristic abnormality except for a rather frequent absence of the activity of disacharidases especially of lactase. A distinct difference of disacharidase was established between the duodenum and the jejunum in some individuals. A systematic study of different levels of the upper gastrointestinal tract established the fact that the activity of brush border enzymes of enterocytes starts to appear in individually different parts of the duodenum and sometimes even as low as in the jejunum. The distribution of lysosomal enzymes and the activity of dehydrogenases display differences as well. Consequently specimens from different parts of the duodenal and jejunal mucosa are not equivalent and cannot be used alternatively for diagnostic purposes. Biopsies of duodenal mucosa are not adequate for the diagnosis of the malabsorption syndrome.
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PMID:Histochemistry of the human duodenal mucosa with special reference to the gradient of activities of the brush border enzymes. 29 9

Crude preparations of hog gastric intrinsic factor or their own previously collected gastric juices administered with labeled vitamin B12 did not enhance vitamin B12 absorption in patients with vitamin B12 malabsorption secondary to pancreatic insufficiency. However, when these sources of gastric intrinsic factor were incubated with three times crystallized preparations of insolubilized bovine trypsin or chymotrypsin, the proteolytic enzymes were removed by centrifugation, and the preparations of gastric intrinsic factor were readministered to these patients, the absorption of vitamin B12 was markedly enhanced. Studies of hog gastric intrinsic factor before and after exposure to proteolytic enzymes failed to show any difference on Sephadex chromatography or polyacrylamide gel electrophoresis or on its affinity for vitamin B12 or the ileal receptor in guinea pigs. These investigations demonstrate that: (1) gastric intrinsic factor as secreted by subjects with pancreatic insufficiency or obtained from hog pyloric mucosal extracts is ineffective in promoting vitamin B12 absorption in patients with pancreatic insufficiency, (2) incubation of crude preparations of gastric intrinsic factor with insolubilized pancreatic proteases modified these preparations of gastric intrinsic factor in an as yet undefined manner, allowing them to enhance vitamin B12 absorption, and (3) in vitro studies using gut sacs or brush border preparations do not reflect the abnormality in vitamin B12 absorption associated with pancreatic dysfunction.
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PMID:Evidence that pancreatic proteases enhance vitamin B12 absorption by acting on curde preparations of hog gastric intrinsic factor and human gastric juice. 31 82

Small intestinal mucosal function and structure was investigated in 13 patients with pernicious anemia prior to and after treatment with vitamin B12. Histological abnormalities of the jejunal mucosa were shortening of villi of varying degree, increased infiltrate of the lamina propria with monocytes and plasma cells and megalocytosis of the absorptive epithelial cell. Malabsorption of d-xylose occurred in 45%, fat in 30%, vitamin B12-IF complex in 69%, hypocarotinemia in 23% and hypoalbuminemia in 30% of the patients. By contrast, digestive brush border enzymes, i.e. disaccharidases, alkaline phosphatase and leucyl-naphthylamidase were not altered in pernicious anemia. Patients with significant jejunal mucosal abnormalities and decrease of the absorptive surface demonstrated malabsorption of one or more nutrients. Morphological and functional abnormalities were restored to normal after treatment with vitamin B12, suggesting that small intestinal changes in pernicious anemia constitute primary systemic manifestations.
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PMID:Functional and morphological abnormalities of the small intestinal mucosa in pernicious anemia--a prospective study. 69 8

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

Absorption of 57Co-labelled vitamin B12 - intrinsic factor (IF) complex and its binding to mucosal precipitate and brush border fractions of rat small intestine was studied in rats pair-fed with a liquid diet containing ethanol 5 g/100 ml, 35% of calories, or isocalorically substituted sucrose. IF was obtained from rats fasted for 18 h. and for each experiment the amount of vitamin B12 added was the minimum required to achieve maximum binding to IF. Rats fed alcohol exhibited hepatic steatosis, proliferation of smooth endoplasmic reticulum, and disordered mitochondria after 6 weeks on the diet, and absorption of vitamin B12, fed with IF by stomach tube, was reduced signficantly. In contrast, binding of 57Co-labelled vitamin B12 -IF complex to mucosal precipitate and brush border fractions was never less than that of fractions from control rats at 4, 8 and 12 weeks on the alcohol diet. Furthermore, binding to the brush border was significantly greater in alcohol-fed rats at 12 weeks whether expressed per unit of beta-naphthylamidase (EC 3.4.1.1) activity or per milligram of protein. Total mucosal sucrase (EC 5.2.1.26) and beta-naphthylamidase were unchanged or slightly increased (beta-naphthylamidase at 12 weeks) on the alcohol-containing diet indicating that total brush border membrane was not reduced. Total brush border binding activity was the same in alcohol-fed and control rats at each time period. These results indicate that malabsorption of vitamin B12 in rats fed alcohol cannot be due to decreased binding of the vitamin B12 - IF complex by brush border membrane receptors, or secondary to a net decrease in membrane receptors.
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PMID:Lack of effect of alcohol on small intestinal binding of the vitamin B12 - intrinsic factor complex. 97 75

Lactase deficiency, manifested clinically by lactose malabsorption, is often the only biochemical evidence of a residual disturbance of jejunal mucosal function after Escherichia coli enteropathy in the infant. Villous morphology is usually normal. A sustained depression of the processes of biochemical differentiation of lactase biosynthesis has been postulated to explain similar states of lactase deficiency, but a possible influence of altered epithelial cell turnover on the mucosal lactase levels has not been investigated. In ten infants with a residual lactose malabsorption, after E. coli infection, jejunal cell renewal activity and disaccharidase activities were studied by analysis of the exfoliated cells collected by lumenal perfusion. Significant increases in DNA and protein exfoliation and in the brush border activities of sucrase and lactase were observed during recovery from the malabsorptive disturbance. DNA and protein efflux increased almost linearly during a 20-day period. Lactase was initially four times more deficient than sucrase activity in the exfoliated cells. Both enzyme activities increased at almost identical rates. Therefore, it took longer for lactase activity to return to normal levels. The lactase/sucrase ratios approached normal at the end of the 20-day period. The changes in the exfoliating levels of the two enzymes, when analysed in relation to the increases in cell renewal activity, suggested a relationship between sucrase and lactase levels and cell age.
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PMID:Intestinal exfoliated cells in infant diarrhoea: changes in cell renewal and disaccharidase activities. 104 54


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