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 present study intended to evaluate the influences of Metagonimus yokogawai on the activities of brush border membrane bound enzymes of the small intestine. Mice were infected with 500 metacercariae respectively, and the worm recovery, morphological changes and enzyme activities were observed chronologically. A part of them were followed after the treatment. Recovered worms decreased in number continuously after the infection, and they were less than 10% after 2 weeks and almost zero after 28 weeks. Villous atrophy and stromal inflammation were found at two locations of the proximal jejunum from 2 weeks to 4 weeks after the infection. The enzymes, alkaline phosphatase, leucine aminopeptidase and disaccharidases (sucrase, lactase, maltase, and trehalase), showed lowered activities in the duodenum and proximal jejunum of the infected mice but they increased in the distal jejunum for the first two weeks. From three weeks after the infection, the activities were gradually recovered. In one week treated mice, they recovered the activities at 2 weeks from the treatment, but there found no differences of the activities between the 3 week treated group and infected controls. The present data reveal that M. yokogawai infection induces degenerative changes of the host's intestinal mucosa not only morphologically but functionally during the initial phase of infection. The lowered enzyme activities in acute metagonimiasis should be associated with malabsorption and diarrhea.
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PMID:Activities of brush border membrane bound enzymes of the small intestine in Metagonimus yokogawai infection in mice. 191 29

Microvillus inclusion disease is an inherited intestinal brush border membrane defect that causes severe fluid and electrolyte malabsorption. In an infant with microvillus inclusion disease (confirmed by electron microscopic evaluation of rectal, jejunal, and gallbladder mucosae), basal stool output was massive (greater than 125 mL . kg-1 . day-1) and was not altered by treatment with clonidine or octreotide. A proximal jejunostomy with mucous fistula was placed, allowing separation of proximal from distal tract outputs (60 mL . kg-1 . day-1 and 100 mL . kg-1 . day-1, respectively). A 10-cm jejunal segment was excised during surgery and mounted in Ussing chambers for determination of transepithelial Na+ and Cl fluxes. Compared with intestine of normal infants, this infant's epithelium showed transmural conductance and unidirectional ion fluxes that were only 30% of normal. With respect to both Na+ and Cl, the excised jejunum was in a net secretory state. Theophylline (5 mmol/L) increased net Cl secretion slightly. In response to mucosal D-glucose (30 mmol/L), jejunal mucosal-to-serosal Na+ flux doubled. In the infant, glucose-electrolyte solution administered intrajejunally did not significantly change stool output, suggesting that all of the solution (40 mL/kg) was absorbed. Subtotal enterocolectomy, in theory, could have decreased purging by 66% in this infant with microvillus inclusion disease, but diarrhea would still have been significant.
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PMID:Microvillus inclusion disease. In vitro jejunal electrolyte transport. 165 50

Glucose/galactose malabsorption (GGM) is an autosomal recessive disease manifesting within the first weeks of life and characterized by a selective failure to absorb dietary glucose and galactose from the intestine. The consequent severe diarrhoea and dehydration are usually fatal unless these sugars are eliminated from the diet. Intestinal biopsies of GGM patients have revealed a specific defect in Na(+)-dependent absorption of glucose in the brush border. Normal glucose absorption is mediated by the Na+/glucose cotransporter in the brush border membrane of the intestinal epithelium. Cellular influx is driven by the transmembrane Na+ electrochemical potential gradient; thereafter the sugar moves to the blood across the basolateral membrane via the facilitated glucose carrier. We have previously cloned and sequenced a Na+/glucose cotransporter from normal human ileum and shown that this gene, SGLT1, resides on the distal q arm of chromosome 22. We have now amplified SGLT1 complementary DNA and genomic DNA from members of a family affected with GGM by the polymerase chain reaction. Sequence analysis of the amplified products has revealed a single missense mutation in SGLT1 which cosegregates with the GGM phenotype and results in a complete loss of Na(+)-dependent glucose transport in Xenopus oocytes injected with this complementary RNA.
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PMID:Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. 200 13

Unexplained bile acid malabsorption associated with diarrhoea that responds to cholestyramine was first described in 1973 but convincing evidence of the proposed mechanism--a defective active ileal bile acid transport--has never been substantiated. Active bile acid transport was quantified in vitro using brush border membrane vesicles prepared from terminal ileal biopsy specimens from 10 patients who fulfilled the criteria of idiopathic bile acid diarrhoea. They were recruited from 181 patients with bile acid malabsorption of various causes. Transport was quantified as in vitro Na+ dependent bile acid transport (INBAT), expressed as pmol taurocholate/mg brush border membrane protein/15 seconds, and in vitro Na+ dependent bile acid local transport capacity (INBALTC), expressed as pmol taurocholate/g ileal biopsy tissue/15 seconds. The lowest INBAT and INBALTC values in the 10 patients with idiopathic bile acid diarrhoea were well above the 10th centile values of a control group of 132 patients. Both INBAT (mean (range) 88 (30-136)) and INBALTC (158 (85-268)) values were significantly higher in the 10 patients than in the control group (INBAT: mean (range) 63 (1-244), INBALTC: mean (range) 98 (1-408)). Quantification of active ileal bile acid transport in these 10 patients with idiopathic bile acid malabsorption suggests that a genetic (carrier) defect is rare in adults.
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PMID:Primary bile acid diarrhoea without an ileal carrier defect: quantification of active bile acid transport across the ileal brush border membrane. 204 Apr 72

The influence of hydrolysis on the assimilation rate of important nutritional carbohydrates was studied in healthy subjects and patients with intestinal diseases, mainly by means of 13CO2 breath test techniques. All substrates were "naturally enriched" with carbon-13. The studies showed that hydrolysis is the rate limiting step for the assimilation of lactose, starch and even maltose, but not for the assimilation of sucrose. The degree of gelatinisation and the degree of side-branching of starch molecules were two important parameters, influencing starch hydrolysis in normal subjects. Addition of wheat bran had no influence on the digestion rate of starch. A comparative study between normal subjects and patients with pancreatic disease, showed that starch digestion may be impaired in patients with pancreatic disease. However, this occurs only if amylase output is extremely low. The effect of lactase deficiency on lactose absorption was studied in patients with a history suggestive of lactase deficiency. For this purpose a lactose 13CO2 and H2 breath test were compared with lactase activity in a jejunal biopsy. The results showed that the relation between lactase activity in the biopsy and lactose assimilation takes the form of a saturation curve. The 13CO2 breath test was found to be a reliable test for the diagnosis of lactase deficiency. Finally, the effect of acarbose on starch digestion was studied in normal subjects, ileostomy patients, and a fecal incubation system. These experiments showed that acarbose may induce an important degree of starch malabsorption. If administered in high doses, the effect is not only related to inhibition of brush border enzymes, but also to the inhibition of alpha-amylase.
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PMID:Georges Brohee Prize 1988-1989. Assimilation of nutritional carbohydrates: influence of hydrolysis. 205 48

The oral inoculation of Giardia lamblia trophozoites (Portland 1 strain) resulted in the establishment of infection by day 3-5 in NMRI mice. By 9-11 days postinfection, the trophozoites load reached maximum (acute phase) and later declined by day 17-21. The tissue sections from infected animals during the establishment phase of infection indicated limited changes in surface epithelium with normal villous length. Although trophozoites of G. lamblia were seen in all sections lying free in the lumen as discrete parasite, the active invasion by the parasite could not be demonstrated. During the acute phase of infection, fuzzy appearance of brush border, marked reduction in villous height and infiltration of intraepithelial lymphocytes were commonly seen in all tissues. Electron microscopic observation demonstrated large numbers of trophozoites of G. lamblia preferentially aggregated at the base of the villi. At some sites, adhesive marks indicating attachment of Giardia trophozoites were also seen by scanning electron microscopy. In addition, severe flattening and blunting of microvilli and occasional loss of basic morphology of intracellular organelles of columnar cells were noticed at the site of parasite colonization under electron microscopy. The brush border microvilli were noted to be damaged in areas where parasites were attached to surface epithelium with the help of suction discs. The morphological changes associated with Giardia infection tended to reverse as the parasite load declined by day 17-21. Thus we feel that malabsorption in giardiasis with total or varying degrees of morphological alterations of surface mucosa can be explained on the basis of reduced absorptive surface area.
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PMID:An ultrastructural analysis of changes in surface architecture of intestinal mucosa following Giardia lamblia infection in mice. 222 57

We used the miniature pig to evaluate the effect of ethanol ingestion on the hydrolysis of pteroylpolyglutamate and on the uptake of pteroylmonoglutamate (PteGlu) by the intestinal brush border membrane, processes that are required for folate absorption. After feeding ethanol or sucrose at 60% of calories for 11 mo, the uptake of PteGlu by jejunal brush-border-membrane vesicles was similar in both groups of animals. Jejunal brush border pteroylpolyglutamate hydrolase was decreased by one-half in the ethanol-fed group. Jejunal brush-border-membrane fluidity, measured by fluorescence polarization, was similar in both groups. Acute exposure of the jejunal vesicles to ethanol increased membrane fluidity and decreased hydrolase activity but had no effect on PteGlu transport. Inhibition of jejunal folate hydrolase by chronic exposure to ethanol may be an early effect in the pathogenesis of folate malabsorption and deficiency in chronic alcoholism.
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PMID:Folate absorption in alcoholic pigs: in vitro hydrolysis and transport at the intestinal brush border membrane. 259 33

Dietary folates exist as pteroylpolyglutamates (PteGlun) that undergo hydrolysis to pteroylmonoglutamate (PteGlu) forms during the process of intestinal absorption. Using the technique of jejunal perfusion of separately labeled folates, our laboratory has demonstrated that hydrolysis of PteGlun occurs on the surface of the jejunum and is a prerequisite for folate absorption. An intestinal brush border pteroylpolyglutamate hydrolase (BB-PPH) has been identified in human and pig jejunum with characteristics that are distinct from those of an intracellular hydrolase (IC-PPH). Functional parallels of BB-PPH with in vivo hydrolysis of PteGlun in human and pig intestine and the clinical responsiveness of BB-PPH to different disease states indicate that this enzyme plays the major physiological role in folate absorption. Folate malabsorption is found in diseases which affect the jejunal mucosa and in response to various drugs. In most of these clinical conditions, folate malabsorption results from suppression of both of the processes of hydrolysis of PteGlun and jejunal uptake of PteGlu. Ongoing studies in miniature pigs are aimed at definition of the sequence of development of folate malabsorption in chronic alcoholism.
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PMID:The intestinal absorption of dietary folates in health and disease. 269 55

Atrophy of the small intestinal mucosa is functionally characterized by a reduction in non-electrolyte transport in vivo. In order to elucidate the cellular defect being responsible for this malabsorption, we have studied the Na+-dependent D-glucose accumulation as well as the activities of aminopeptidase M and maltase in brush border membrane vesicles prepared from jejunal self-emptying blind loops and corresponding intestinal segments of sham-operated control rats. Membrane vesicles from atrophic mucosa did not show any differences in D-glucose uptake or in enzyme activities when compared with those derived from normal intestine. Thus it is unlikely that the impaired non-electrolyte absorption in the atrophic mucosa in vivo is due to a defect in cellular transport processes. It is more probable that the functional impairment is the result of the diminished absorptive surface in this pathophysiological condition.
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PMID:[Functional characterization of luminal enterocyte membranes of the small intestine mucosa using isolated brush border membranes]. 288 Apr 30

NMRI mice immunosuppressed with dexamethasone followed by challenge intraesophageally with axenic Giardia lamblia (Portland I) trophozoites had severe infection in terms of the trophozoite counts in the jejunum. Although the immunosuppressive treatment with cortisone itself resulted in a deleterious effect on brush border membrane enzymes, the decline in disaccharidases (sucrase, maltase, and lactase) and alkaline phosphatase was highly significant (P less than 0.001) following G. lamblia infection. The alterations in enzymatic activity in immune intact but infected animals demonstrated the potential of the parasite itself to cause damage to the brush border membrane. We believe that individuals with underlying immunodeficiency, upon infection with G. lamblia, may have increased damage of the brush border membrane, leading to severe malabsorption.
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PMID:Giardia lamblia infection in immunosuppressed animals causes severe alterations to brush border membrane enzymes. 276 19


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