title: Sequential disaccharidase loss in rat intestinal blind loops: impact of malnutrition.
abstract: 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.
authors.forename: P
authors.initials: P
authors.lastname: Sherman
authors.forename: A
authors.initials: A
authors.lastname: Wesley
authors.forename: G
authors.initials: G
authors.lastname: Forstner
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000188:drug therapy / Q000201:enzymology*; D005696:Galactosidases / Q000378:metabolism*; D005959:Glucosidases / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000201:enzymology*; D007583:Jejunum / Q000201:enzymology / Q000382:microbiology*; D008034:Lincomycin / Q000627:therapeutic use; D008297:Male; D008871:Microvilli / Q000201:enzymology; D009748:Nutrition Disorders / Q000201:enzymology*; D051381:Rats; D011919:Rats, Inbred Strains; D013047:Specific Pathogen-Free Organisms; D013393:Sucrase / Q000378:metabolism*; D013997:Time Factors; D000520:alpha-Glucosidases / Q000378:metabolism*; D001616:beta-Galactosidase / Q000378:metabolism*
chemical_list: D008034:Lincomycin; D005696:Galactosidases; D005959:Glucosidases; D000520:alpha-Glucosidases; D001616:beta-Galactosidase; D013393:Sucrase