Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.26 (invertase)
 4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To better understand the pathogenesis of infantile viral gastroenteritis, we studied Na+ and Cl- fluxes in vitro in short-circuited jejunal epithelium from 8-10-day-old piglets after infection with a standard dose of human rotavirus given via nasogastric tube. 11 infected piglets, all of whom became ill, were compared with 9 uninfected, healthy litter-mates. When killed 72 h after infection, intestinal villi were shorter and crypts deeper (P less than 0.025) in duodenum, upper jejunum, and mid-small intestine, but not ileum in infected piglets. Virus antigen was seen by fluorescence microscopy in occasional jejunal villus tip cells in only four infected piglets and no controls at 72 h. Net Na+ and Cl- fluxes did not differ from noninfected litter-mate controls under basal conditions, but response to glucose was blunted in infected piglets (P less than 0.001). Theophylline stimulated net Cl- secretion in both infected and control animals, and cyclic AMP concentration in isolated jejunal villus enterocytes did not differ significantly. In isolated jejunal villus enterocytes of infected piglets, thymidine kinase activity increased (P less than 0.001), and sucrase activity decreased (P less than 0.001). We conclude that in this invasive enteritis caused by a major human viral pathogen, glucose-coupled Na+ transport is impaired in the jejunum at a time when the villus epithelium shows enzyme characteristics of crypt epithelium, and when little or no virus is present. These findings are identical to those occurring in an invasive coronavirus enteritis of piglets but differ markedly from those seen with enterotoxigenic diarrhea.
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PMID:Human rotavirus enteritis induced in conventional piglets. Intestinal structure and transport. 19 22

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

To investigate the effect of chronic protein-calorie malnutrition on intestinal repair after an enteric infection, we examined small intestinal structure, enzyme activity, and sodium transport in undernourished piglets during the acute and convalescent phases of a viral enteritis, transmissible gastroenteritis (TGE). Gnotobiotic pigs, nutritionally deprived from the age of 7 days, gained less weight than dietary controls from 14 days of age until the end of the study. Animals from malnourished and control diet groups were inoculated with TGE virus at 22-23 days and studied during the acute (40 h) and convalescent (4, 10, and 15 days) stages of this experimental enteritis along with noninfected dietary controls. After TGE infection, we observed a further decrease in weight gain and an increased mortality only in undernourished pigs. In jejunum and ileum of both dietary groups at 40 h after TGE infection, we observed comparable structural lesions, similar decreased activities of mucosal enzymes (sucrase, lactase, sodium-potassium-dependent ATPase), and increased thymidine kinase activities. Also we noted comparable diminution of glucose-stimulated jejunal sodium absorption in both dietary groups at 40 h. In control diet pigs, transport abnormalities recovered by 4 days after TGE infection and normal mucosal structure and enzyme activity returned over 4-15 days. In undernourished piglets, structural repair and enzyme abnormalities were prolonged when compared with the control diet group; glucose-stimulated sodium transport did not recover until 10 days after infection and never regained the enhanced activity seen in noninfected undernourished controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of chronic protein-calorie malnutrition on small intestinal repair after acute viral enteritis: a study in gnotobiotic piglets. 392 24

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 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