Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.108 (lactase)
 2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were undertaken to determine the relationship of intestinal disaccharidase activity to age and race, and the relationship of mucosal damage to a primary low lactase activity. The first study consisted of data on 399 persons (339 whites, 53 blacks, and 7 American Indians) ages 1 month to 93 years, with normal intestinal histology. Among whites, all 117 children 5 years old or under had high lactase levels, whereas low levels were found only in subjects over 5 years of age. No low lactase levels were identified among the 11 black children 3 years old or under, but in comparison to coetaneous white children, their mean lactase activity was signficantly less. The majority of older blacks had low lactases. In whites and blacks alpha-disaccharidases did not participate in the age-related changes demonstrated with lactase. Of the 7 American Indians, none under 26 months old had low lactase levels, whereas the 4 over 10 years old had low activities. Heterozygotes for sucrase-isomaltase deficiency were identified only among whites. Low lactase levels developed during childhood in all races studied, however, many for unknown reasons maintained their lactose tolerance until adulthood. In the second study of 13 additional children with secondary disaccharidase deficiencies, emergence of a primary low lactase was related to age and race, rather than to mucosal damage. It appears that primary low intestinal lactase levels are absent or rare in whites under 5 and blacks under 3 years of age, and the deficiency is not related to mucosal damage.
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PMID:Intestinal disaccharidase activities in relation to age, race, and mucosal damage. 10 Mar 68

Bacterial extracts were prepared from cultures originating in chronic self-filling intestinal blind loops in rats. Their ability to remove active maltase molecules from isolated brush border membranes was studied in vitro. Twelve strains in 51 tested, belonging to one of three species, Bacteroides fragilis, Clostridium perfringens, and Streptococcus fecalis, possessed maltase-releasing activity. The ability to remove maltase correlated well with the ability to hydrolyze p-nitrophenyl-tert-butyloxycarbonyl-l-alaninate (NBA), an ester substrate rapidly hydrolyzed by elastase, but not with substrated favored by tryhsin and chymotrypsin. Maltase-releasing activity from C. perfringens was strongly inhibited by soybean trypsin inhibitor and to a lesser extent by lima bean trypsin inhibitor. Of four chloromethylketone active-site directed inhibitors tested with specificities for elastase, trypsin, and chymotrypsin, inhibition was maximal with elastase-specific inhibitors. In two species, activity was shown to be heat sensitive, and to be inhibited by concentration of the extract. In one species maltase-releasing activity was shown to be due to an enzyme of molecular weight at least 66,000 with the capacity to remove lactase, sucrase, and alkaline phosphatase, as well as maltase. The results indicate that anaerobic or facultatively anaerobic species, previously identified with the pathology of of the blind loop syndrome, contain proteases which are capable of removing components of the intestinal surface membrane. These proteases appear to have elastase-like substrate specificity and may be involved in the etiology of disaccharidase deficiency in bacterial overgrowth syndromes.
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PMID:Pathogenesis of mucosal injury in the blind loop syndrome. 35

7 infants, aged 5 weeks to 11 months, with clinically documented intolerance to cow's milk protein, chronic diarrhea, and failure to thrive, underwent small intestinal (peroal, suction) biopsy before and after withdrawal of milk proteins. Mucosal specimens were examined by light microscopy and assayed for disaccharidase activities. In all patients, moderate to severe mucosal changes were presented, associated with marked inflammation of lamina propria and damages to the brushborder. Disaccharidase activities (lactase, sucrase, maltase and palatinase) were markedly depressed in all. Follow-up biopsies were obtained in 6 infants, after 3-5 months on a milk-protein-free diet. At the time of the second biopsy, the disaccharidase activities had risen significantly and histologic improvement had occurred in each instance. In infancy, intestinal mucosal lesions due to intolerance to cow's milk protein are histologically indistinguishable from those seen in gluten-sensitive enteropathy and are associated with marked secondary disaccharidase deficiencies. Following therapy, the activity of the disaccharidases become normal or near normal prior to the complete morphologic recovery of the small intestinal mucosa.
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PMID:Disaccharidase deficiency in infants with cow's milk protein intolerance. Response to treatment. 62 28

Jejunal biopsies from 19 adult Greenland Eskimos were studied regarding disaccharidases, two intracellular beta-galactosidases, and morphological appearance. Fifteen of the patients (79%) had low lactase activity, and 3 of these (16%) had sucrase-isomaltase deficiency as well. Two patients had low trehalase activity. Microscopical appearance was essentially normal in all the biopsies, except for a certain stromal plasma cell infiltration. All the patients with low lactase activity had a measurable residual activity of brush border lactase, which was localized in the middle and apical parts of villi, as normally seen for digestive enzymes. Lysosomal acid beta-galactosidase and cytosol hetero beta-galactosidase were not altered. In the patients with sucrase-isomaltase deficiency there was a complete absence of active sucrase-isomaltase complex. The residual maltase, as well as the very weak residual isomaltase, was exerted exclusively by the heat stable maltases (maltase II and III). The material is the first one in which multiple, but not generalized disaccharidase deficiencies are demonstrated.
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PMID:Intestinal disaccharidases in Greenland Eskimos. 115 47

Intestinal disaccharidase activities were determined in 294 jejunal biopsies obtained from 254 children with various disorders of the small bowel, and alkaline phosphatase activity was measured in 251 biopsies. In normal mucosa a broad range of enzyme activity was found corresponding with the data in the literature. A primary disaccharidase deficiency was observed in 5 children with congenital sucrase-isomaltase deficiency and in a 12-year-old Egyptian boy with acquired lactase deficiency. A secondary generalized depression of disaccharidase activity and a diminution of alkaline phosphatase activity existed chiefly in patients who had severe or moderate mucosal damage, also in active coeliac disease and during gluten loading, in protracted diarrhoea of infancy, chronic malabsorption of unknown origin and agammaglobulinemia. During remissions enzyme activities recovered together with mucosal improvement. Low levels of enzyme activities were also seen in some cases of protracted diarrhoea of infancy and chronic malabsorption of unknown origin although only mild mucosal lesions were demonstrated.
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PMID:[Intestinal disaccharidase and alkaline phosphatase activities of jejunal biopsies in small bowel diseases of children (author's transl)]. 127 85

The activities of four disaccharidases were examined in resistant (C57Bl/6) and susceptible (C3H/HeN) mice during the primary infection with Giardia muris and after challenge with either trophozoite extract or cysts. Significant decreases in lactase, sucrase, trehalase, and maltase activities in C57Bl/6 mice and lactase and sucrase activities in C3H/HeN mice in the anterior 25% of the small intestine were observed on day 10 after infection. The activities of maltase, sucrase, trehalase, and lactase in the jejunum of C3H/HeN mice were significantly reduced after challenge with trophozoite extract, when compared with the uninfected or infected, but not challenged animals. Decreases in enzyme activities of C3H/HeN mice were evident as early as 12 hours after challenge with the extract. The resistant C57Bl/6 mice showed little change in disaccharidase activity after challenge with trophozoite extract. On the other hand, challenge with cysts resulted in a few decreases in disaccharidase activities in both strains of mice: C57Bl/6 mice showed decreases in the duodenum, while disaccharidases of C3H/HeN mice had lower activity more posteriorly. Thus, challenge with parasite antigen results in a more severe disaccharidase deficiency in susceptible hosts when compared with resistant ones.
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PMID:Disaccharidase activity in the small intestine of susceptible and resistant mice after primary and challenge infections with Giardia muris. 153 93

Investigation of intestinal disaccharide hydrolysis and permeability by means of a non-invasive differential sugar absorption test was performed in a family containing two siblings with primary sucrase-isomaltase deficiency. The procedure, which depends on measurement of urinary excretion ratios after the oral administration of lactose, sucrose, palatinose, lactulose and L-rhamnose, is capable of simultaneous determination of intestinal lactase, sucrase, and isomaltase activity and lactulose:rhamnose permeability. The results corresponded well with those of disaccharidase assay and histological findings in jejunal biopsy tissue obtained from the patients. Palatinose proved a satisfactory substrate for in vivo assessment of intestinal isomaltase activity. The method described provides a reliable and comprehensive assessment of intestinal disaccharide hydrolysis, and simultaneous estimation of permeability assists discrimination of primary from secondary disaccharidase deficiency. The ability to assess three different disaccharidase activities in addition to intestinal permeability by means of a single test, and the simplicity of preservation and transport of urine samples for sugar analysis, makes this a convenient, definitive method for the investigation of defective sugar absorption in both patients and population groups.
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PMID:Combined assessment of intestinal disaccharidases in congenital asucrasia by differential urinary disaccharide excretion. 237 Mar 9

Seven patients with congenital sucrase-isomaltase deficiency corresponding to the known diagnostic criteria and five patients having combined disaccharidase deficiencies with unusual pattern characterized by more pronounced sucrase than lactase deficiency were found among 505 children investigated by first jejunal biopsy. On the base of the case histories, the complications and the comparative evaluation of patient and control groups' data (the latter consisted of nine untreated coeliacs) the congenital sucrase-isomaltase deficiency was found to make the patients to be especially susceptible to enteral infections and consequently to postinfectious intestinal damages. These complicated cases do not correspond to the classic diagnostic criteria of the congenital enzyme deficiency causing diagnostic errors. In order to avoid the misdiagnoses the authors suggest modification of the diagnostic criteria of congenital sucrase-isomaltase deficiency as follows: the diagnosis of congenital enzyme deficiency might be verified in spite of mild histological signs and hypolactasia if the degree of lactase deficiency repeatedly and significantly is exceeded by the degree of sucrase deficiency.
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PMID:[Congenital saccharase-isomaltase defect--diagnostic difficulties]. 251 45

We studied lactase, maltase, and sucrase activities in the mucosa of self-filling blind loops (SFBL) in adult rats at weekly intervals after SFBL formation in order to determine the sequence in which disaccharidase activities fall. The studies were carried out on nourished and malnourished rats and extended to a recovery period induced by antibiotics to determine the effects of malnutrition on the establishment and repair of disaccharidase deficiencies caused by bacterial overgrowth. Malnutrition was produced by feeding 50% of the intake of paired rats fed ad libitum. Disaccharidase activities were determined in SFBL from nourished and malnourished rats at 7-day intervals until pandisaccharidase deficiency was established and during a 2-wk recovery period induced by antibiotics. Maximal SFBL bacterial counts in both nourished and malnourished groups of rats and brush-border glycoprotein degradation ratios were established at 7 days. In nourished rats only lactase was deficient at 7 days; maltase and sucrase fell later and sequentially. In malnourished rats all three disaccharidases were reduced at 7 days. Disaccharidase activities in self-emptying blind loops (SEBL), used as operated controls, were not decreased 28 days after surgery. Malnutrition had no effect on disaccharidase activities in the SEBL, and malnutrition did not affect recovery rates with antibiotic therapy. We conclude that small intestinal bacterial overgrowth causes a staggered loss of disaccharidase activities beginning with the loss of lactase activity. In the presence of bacterial overgrowth, malnutrition accelerates the conversion of a mono- to a pan-disaccharidase deficiency.
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PMID:Sequential disaccharidase loss in rat intestinal blind loops: impact of malnutrition. 315 66

Sucrase-isomaltase deficiency is an inherited disaccharidase deficiency that leads to malabsorption of sucrose, with resulting diarrhea and abdominal distention and cramps. We investigated the sucrose-splitting effect of viable yeast cells in eight children with congenital sucrase-isomaltase deficiency, by means of the sucrose hydrogen breath test. This test is based on the fact that hydrogen is released from the malabsorbed sucrose by the colonic microflora. We found that 0.3 g of lyophilized Saccharomyces cerevisiae, given after loading with 2 g of sucrose per kilogram of body weight, reduced hydrogen excretion in all patients, on average by 70 percent, in parallel with a complete loss or evident reduction of clinical symptoms. In vitro, lyophilized and fresh S. cerevisiae (fresh baker's yeast) had appreciable sucrase activity, a low isomaltase and maltase activity, and virtually no lactase activity. The sucrase activity was more inhibited by undiluted than by diluted gastric juice. We conclude that patients with congenital sucrase-isomaltase deficiency who intentionally or unintentionally consume sucrose can ameliorate the malabsorption by subsequently ingesting a small amount of viable yeast cells, preferably on a full stomach.
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PMID:Enzyme-substitution therapy with the yeast Saccharomyces cerevisiae in congenital sucrase-isomaltase deficiency. 355 46


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