Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.20 (alpha-glucosidase)
 4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of cows' milk protein (CMP) on the mucosal disaccharidases was investigated in 23 infants with acute infective enteritis. Jejunal biopsies performed before and after cows' milk provocation were subjected to histological examination and to mucosal disaccharidase enzyme (lactase, sucrase, and maltase) analyses. After milk challenge, changes in mucosal histology were observed in 18 infants, in 17 of them the levels of all 3 mucosal disaccharidases were much reduced. 10 of these infants developed diarrhoea and, in 6, the stools were positive for reducing sugar. It is concluded that CMP has a deleterious effect on the jejunal mucosa of young infants recovering from infective enteritis, so that in the management of young infants with sugar intolerance secondary to infective enteritis, CMP and lactose should be excluded from the diet.
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PMID:Cows' milk protein-sensitive enteropathy: an important contributing cause of secondary sugar intolerance in young infants with acute infective enteritis. 57 Mar 76

In infants suffering from protein-calorie malnutrition, the decreased intestinal mucosal lactase specific activity could be due either to the protein-calorie malnutrition or to the commonly associated enteritis (viral or bacterial) and intestinal parasites. We studied intestinal mucosal disaccharidase (lactase, sucrase, and maltase) specific activity in suckling (1 and 2 wk old), weanling (3 wk old), and postweaning (4 and 6 wk old) control and growth-retarded (malnourished) rats. Growth retardation was induced by feeding mother rats and postweaning rats a diet deficient in protein. In the malnourished rats, with few exceptions, specific activity of the disaccharidases in the intestinal mucosa were similar to those in the corresponding control groups of rats. However, because of marked mucosal atrophy total intestinal mucosal disaccharidase activities were more than 50% lower in the malnourished rats. These findings suggest that the specific activity of the intestinal mucosal disaccharidases is not affected by malnutrition per se.
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PMID:Intestinal disaccharidases in malnourished infant rats. 679 98

The paper is concerned with the results of morphological and biochemical studies of the duodenum and ileum in young rabbits with salmonellosis. It was shown that all the parts of the small intestine were involved into the pathological process. Enzymopathy developed in the presence of acute catarrhal inflammation and erosive enteritis accompanied by ulceration of necrotized lymph follicles of Peyer's patches of the small intestine. The activity of maltase and alkaline phosphatase was found to be most vulnerable. Of crucial significance in the development of diarrhea in experimental young rabbits were pronounced morphological alterations and derangement of enzyme-forming function in the small intestine.
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PMID:[State of the small intestine in rabbits with salmonella infections]. 703 5

The effect of enteritis on the development of the small intestine was examined in newborn, colostrum-deprived piglets infected with a human isolate of Y. enterocolitica (serotype 0:3, biotype 4) soon after birth. The piglets were killed 3 days (n = 6) or 5 days (n = 8) after infection, or antibiotic therapy was commenced on day 5 and the animals killed on day 14 (n = 5). Compared with the non-infected controls, infected animals had reduced mucosal lactase and sucrase, but not maltase activity, while after antibiotic therapy, previously infected piglets had a lower lactase and a higher maltase and sucrase activity. Lactase activity was significantly reduced in the duodenum and jejunum, and mean values were lower in the ileum, but the difference did not reach significance; maltase activity was greater at all ages from the distal jejunum to the mid-ileum; sucrase activity was reduced in all segments up to day 5 but after antibiotic therapy was increased in the jejunum and appeared early in the ileum. Enzyme profiles were more mature along the crypt-villus axis in some segments of the intestine in previously infected piglets. Sodium-potassium-ATPase activity was unchanged. There was a reduced villus height:crypt depth ratio, crypt hyperplasia and increased crypt cell proliferation. Morphological maturation, indicated by loss of vacuoles and location of the nucleus at the base of the enterocyte, proceeded distally from the duodenum to ileum from 3 to 14 days of age when only the ileum remained immature. In infected piglets, there was reduced vacuolation and earlier location of the nucleus at the base of the cell in the distal intestine. Accelerated maturity of specific disaccharidases and enterocyte morphology in infected piglets appears to be due to physical damage to the mucosa resulting in faster proliferation of crypt cells and migration of enterocytes. It is suggested that this may reduce macromolecular internalisation and impair the ability to utilise dietary carbohydrate and may have long-term effects on growth and immunological responses of the gut.
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PMID:Impact of Yersinia enterocolitica enteritis on disaccharidase activity and small intestinal morphology in colostrum-deprived newborn piglets. 1603 44