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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protein, fat and carbohydrate absorption in preterm infants fed on human milk or formulae are reviewed. Even in the most premature infants absorption of protein is satisfactory. Nitrogen net absorption is about 85-90% of intake and results slightly lower with human milk than with formulae. The lower apparent digestibility of human milk is probably due to the poorly degraded IgA immunoglobulins and the rapid transit time. Lactose is well tolerated by the preterm infants despite the low lactase activity at birth. Glucose polymers, which have a low osmotic activity and are suitable for increasing carbohydrate intake of formulae, are well absorbed probably for the activity of salivary amylase and brush border glucoamylase, which have been shown to be well developed at birth. Premature infants absorb fat poorly. This malabsorption that increases with the lowering of gestational age is due to low pancreatic lipase activity and to low intraluminal concentration of bile salts. Due to its bile stimulated lipase activity, non-heat-treated human milk used at least in part is an effective method to improve fat absorption in preterm infants. Faecal energy determined using a calorimetric bomb appears to be a simple and an accurate method to predict faecal fat and avoiding expensive and cumbersome analysis.
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PMID:[Absorption of proteins, carbohydrates and fats in the preterm neonate]. 357 19

Jejunal biopsies from six patients having the small bowel enteropathy associated with common variable immunodeficiency have been subjected to analytical subcellular fractionation and enzymic and regulatory peptide microassay to define the organelle pathology of this syndrome. Compared with normal subjects, the immunodeficient patients had decreased activities of the three brush border enzymes: alkaline phosphatase, gamma-glutamyl transferase and alpha-glucosidase. The other organelle marker enzyme activities and all the regulatory peptide concentrations did not differ from the controls. Density gradient experiments showed a complete loss of particulate beta-glucosidase (lactase) with activity entirely located in the cytosol. The integrity of other organelles was normal. These data indicate that the enteropathy of common variable immunodeficiency is associated with abnormalities in the jejunal brush border analogous to those present in tropical malabsorption syndrome.
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PMID:Jejunal mucosal enzyme activities, regulatory peptides and organelle pathology of the enteropathy of common variable immunodeficiency. 369 46

Two new reversible inhibitors of intestinal alpha-glycosidases (BAY m1099 & o1248) have been derived from deoxynojirimycin. Their inhibitory substrate specificity has been investigated in man using test meals of the dietary carbohydrates, sucrose, maltose, and starch. Both inhibitors abolished the postprandial glycaemic rise after sucrose and m1099 50 mg did after maltose and starch, whereas o1248 20 mg had no effect after maltose and only a small effect after starch. Breath hydrogen evolution, as an indirect measure of malabsorption, showed that the reduced glycaemic responses, particularly after sucrose, were associated with considerable substrate malabsorption. Dose response studies showed that lower doses of both inhibitors could reduce postprandial glycaemia significantly without causing malabsorption. Both inhibitors were tolerated well. These two new enzyme inhibitors have different substrate specificity in man and can, in appropriate dose, regulate postprandial glycaemia by selective inhibition of brush border enzymes without causing malabsorption. In addition to their therapeutic importance, they provide a valuable experimental model of specific intestinal enzyme deficiency states.
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PMID:Regulation of the absorption of dietary carbohydrate in man by two new glycosidase inhibitors. 380 23

The bacterial overgrowth syndrome constitutes an intestinal problem involving alterations in motility and injury to the brush border and mucosa. The overgrowth of bacteria also causes secretion, malabsorption, and maldigestion. These alterations result in a clinical syndrome that manifests itself as weight loss, malabsorption of specific nutrients, and (usually) diarrhea. There are known causes of bacterial overgrowth, such as intestinal diverticuli or surgical procedures involving a vagotomy, but in our experience most cases remain idiopathic. This review evaluates the mechanisms of bacterial overgrowth, as currently understood, and specifically addresses the known causes of diarrhea that results from bacterial contamination of the small intestine.
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PMID:Review: pathophysiology of diarrhea caused by bacterial overgrowth of the small intestine. 389 May 41

Acarbose is an alpha-glucosidase inhibitor which reversibly and competitively inhibits the digestion of oligo- and disaccharides at the brush border of the small intestine. This study evaluates the preventive and therapeutic properties of acarbose in the treatment of obesity. Dose-response experiments were performed during repeated sucrose loads in man in order to investigate the effects of acarbose on plasma insulin and blood glucose levels. After titration of efficient doses, a long-term tolerance test of acarbose was undertaken in a small pilot study. Finally, the relapse preventing effect of acarbose was tested during double-blind cross-over conditions in 24 weight reduced obese women. In growing Sprague-Dawley rats, the effects of acarbose on body weight, lipid depots and adipose tissue cellularity were tested during pair-feeding and ad libitum conditions. Such effects were also studied in adult ad libitum-fed rats. Blood glucose, plasma insulin, body fat, depot lipids as well as fat cell weight and number were determined with established techniques. During a sucrose load, acarbose reduced insulin in a dose-dependent fashion. Glucose was also reduced, but not dose-dependently and only to a moderate extent. During a 200 g sucrose load, 400 mg of acarbose did not necessarily result in a maximal reduction of the insulin response while the glucose response was maximally inhibited after 100 mg. Acarbose reduced the relapse rate after weight reduction. No serious side effects were observed. Flatulence and meteorism occurred frequently. In growing rats, acarbose retarded the development of body weight and of lipid depots not only during pair-feeding conditions but also in ad libitum-fed animals eating considerably more than their controls. The spontaneous food consumption was increased by acarbose also in adult rats but in these animals neither body weight nor lipid depots were significantly reduced by acarbose. It is concluded that acarbose induces a carbohydrate malabsorption. Insulin levels are reduced not only via a decreased glycemic stimulus but also by interference with other insulin releasing mechanism(s). Acarbose is the first drug ever tested with long-term relapse reducing effects after weight reduction. Animal experiments suggest that acarbose may be of value in the prevention of obesity, particularly since the drug retards lipid accumulation also during ad libitum-feeding.
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PMID:alpha-Glucosidase inhibition in obesity. 391 27

Incorporation of purified phytohemagglutinin (PHA) lectins derived from red kidney beans (Phaseolus vulgaris) in the diet of weanling rats will cause growth failure, malabsorption of nutrients, and bacterial overgrowth in the small intestine. These effects are not caused by feeding a similar quantity of PHA to germfree rats. To define the morphological and bacterial changes on the mucosal surfaces of the jejunum, ileum, and cecum in greater detail, we pair fed two groups of weanling rats isocaloric, isonitrogenous diets with or without 0.5% PHA protein. On the jejunal surfaces of control rats, the mucous layer was a confluent covering with sparsely scattered bacteria and protozoa. In PHA-treated rats, the mucous layer was thin and discontinuous, and the microvillous surface of the tissue was extensively populated by bacterial cells of two distinct morphotypes--a gram-negative rod and a gram-positive coccobacillus. In all PHA-treated animals, these bacteria formed adherent monospecific or mixed adherent microcolonies on the tissue surface. Tissue damage was observed in PHA-exposed jejunal tissue as evidenced by vesiculation of the microvillous plasma membrane and by damage to the brush border membrane. On the ileal surfaces of control rats, there was a thick mucous layer within which small numbers of bacteria and protozoa were seen. Segmented filamentous bacteria were anchored in the tissue surface. In PHA-treated rats, the ileal surface was only incompletely covered by a mucous layer, and the overlying mucosal surface was extensively covered by large numbers of protozoan cells (predominantly Hexamita muris). Most of the ileal surfaces not covered by the mucous layer were occupied and virtually occluded by an overgrowth of these protozoan cells with occasional cells of Giardia muris and the tissue-associated segmented bacillus. In the ceca of control rats, the mucosa was incompletely covered by a discontinuous mucous layer and colonized by an unnamed Spirillum sp., other bacteria, and occasional protozoa. The cecal surfaces of PHA-treated rats retained most of their incomplete overlying mucous layer, which was heavily colonized by the same type of Spirillum sp. seen in untreated animals; intestinal crypts were colonized. These descriptive morphological studies demonstrate that exposure to purified PHA in the diet caused characteristic changes in the microbial ecology of the small intestine. The changes in microbial flora contributed to the malabsorption of nutrients in the small intestines of PHA-fed animals.
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PMID:Intestinal microbial flora after feeding phytohemagglutinin lectins (Phaseolus vulgaris) to rats. 402 92

Chronic diarrhoea is frequent in acquired immune deficiency syndrome (AIDS) but has been poorly investigated so far. We report four patients with AIDS in whom diarrhoea and malabsorption were outstanding features, and who underwent extensive digestive investigations. Diarrhoea was a presenting symptom in all subjects and was of secretory type in three of them. D-xylose and vitamin B12 were malabsorbed in all cases; steatorrhea was found in the two patients who could ingest significant amounts of fat. Faecal alpha 1-antitrypsin clearance was increased in all subjects. Search for digestive pathogens showed unusual protozoans in all patients: in case 1, optical and electron microscopy revealed the presence in the cytoplasm of villous enterocytes of Microsporidia protozoans still unreported in AIDS. Stool and jejunal fluid examination showed Isospora belli in case 2 and Cryptosporidium in cases 3 and 4. On histological and ultrastructural study the former was localised in the cytoplasm of a few enterocytes and the latter was scattered throughout the villus and crypt brush border. Otherwise small intestinal histology only showed minor non-specific changes and the enterocytes were ultrastructurally normal. In patient 3 the slow marker intestinal perfusion technique showed a profuse fluid secretion in the duodenum and proximal jejunum. All patients needed prolonged total parenteral nutrition. Cryptosporidium and Microsporidia could not be eradicated despite multiple drug trials. Isospora belli was transiently cured by pyrimethamine-sulphadiazine. Only patient 2 is presently at home, and patients 1, 3, and 4 died after two, six, and nine months of total parenteral nutrition, respectively.
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PMID:Diarrhoea and malabsorption in acquired immune deficiency syndrome: a study of four cases with special emphasis on opportunistic protozoan infestations. 403 92

We review here the case histories and results of in vivo and in vitro tests for eight children with congenital selective glucose and galactose malabsorption (GGM) whom our laboratory has followed up since 1971. Clinically, GGM was manifested by intractable, acidic, sugar-containing diarrhea that started during the neonatal period. Diarrhea only abated when glucose and galactose were removed from the diet. The disease was notable for the absence of other symptoms, although mellituria was a common finding. Defective sugar transport was permanent, but sugar tolerance appeared to increase with age. In vitro, intracellular mucosal glucose concentration (C) was significantly below control level in GGM intestinal tissue for concentrations (M) of 10 and 0.1 mM glucose in the medium. C/M for galactose also decreased, while the C/M ratios for alanine and xylose were within the control range. Glucose influxes across the luminal membrane, net glucose transepithelial fluxes, and electrical parameters were all consistent with defective sodium and glucose cotransport at the brush border membrane of jejunal epithelial cells. However, the present results are also consistent with a small residual active transport system observed only at low glucose concentration in the medium. Further observations are needed to establish the role of glucose transport systems in absorption of other monosaccharides, the relationship between kidney and intestinal sodium-glucose cotransport systems, and their genetic control.
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PMID:Congenital selective malabsorption of glucose and galactose. 406 75

Human jejunal brush border folate conjugase (EC 3.4.22.-) was partially purified and characterized. Three drugs known to be associated with clinical folate deficiency were tested for inhibition of the partially purified enzyme. Using jejunal mucosa from obese patients undergoing intestinal bypass surgery, brush border folate conjugase was purified 50-80-fold by centrifugation, Triton X-100 solubilization and DEAE-Sephadex and Sephacryl S-200 chromatography. Using synthetic pteroyldiglutamyl[14C]glutamate as substrate, the enzyme was found to have a pH optimum of 6.5 and an apparent Km of 1.6 micro M. Incubation of the enzyme with synthetic pteroyl[14C]glutamylhexaglutamate resulted in a spectrum of shorter-chain 14C-labeled pteroylglutamates at 60 min. Pteroyl[14C]glutamate was the major product at 120 min, with quantitative recovery of free glutamate in the incubation medium. Salicylazosulfapyridine was a competitive inhibitor of the enzyme (Ki = 0.13 mM), while ethanol, diphenylhydantoin and salicylazosulfapyridine metabolites had no effect. These data suggest that brush border folate conjugase is an exopeptidase which progressively hydrolyzes glutamyl units from pteroylpolyglutamate, leaving pteroylmonoglutamate as the folate form available for intestinal transport. Inhibition of brush border folate conjugase by salicylazosulfapyridine provides a mechanism for folate malabsorption and deficiency in chronic users of this drug.
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PMID:Human jejunal brush border folate conjugase. Characteristics and inhibition by salicylazosulfapyridine. 611 48

In the United States and other developed countries thiamin deficiency is often related to chronic alcoholism. A number of mechanisms may be involved in the pathogenesis of thiamin deficiency in the alcoholic population. An important cause is inadequate intake of thiamin. Moreover, there may be decreased converstion of thiamin to the active coenzyme, reduced hepatic storage of the vitamin in patients with fatty metamorphosis, ethanol inhibition of intestinal thiamin transport, and impaired thiamin absorption secondary to other states of nutritional deficiency. The present discussion focuses on the mechanism of ethanol-related thiamin malabsorption. Under normal conditions thiamin transport in animals and humans is biphasic. At low or physiological thiamin concentrations, transport is a saturable, carrier-mediated, active process; but at higher concentrations, the transport of thiamin is predominantly passive. Ethanol reduces the rate of intestinal absorption and the net transmural flux of thiamin. Furthermore, ethanol inhibits only the active and not the passive component of thiamin transport by impeding the cellular exit of thiamin across the basolateral or serosal membrane. The impairment of thiamin movement out of the enterocyte correlates with a fall in the activity of Na-K ATPase. Bound to the basolateral membrane, Na-K ATPase is believed to be involved in the kinetics of active transport. Ethanol also increases the fluidity of enterocyte brush border and basolateral membranes. Since ethanol increases membrane fluidity it is possible that tahe impairment of thiamin transport and the diminution of Na-K ATPase activity may be related, at least partly, to a physical perturbation of the enterocyte membrane.
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PMID:Mechanisms of thiamin deficiency in chronic alcoholism. 625 54


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