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- W2034160802 abstract "Objective The authors investigated the role of mucin and secretory immunoglobulin A (sigA) in a model of nutritionally induced bacterial translocation. Background Parenteral and certain elemental diets have been shown to impair intestinal barrier function, whereas fiber has been shown to protect against nutritionally induced bacterial translocation. However, the factors responsible for these phenomenon have not been fully determined. Methods Intestinal mucin levels, mucosal protein content, slgA, intestinal morphology, and permeability to horseradish peroxidase, bacterial translocation, and intestinal bacterial population levels were measured in rats 7 days after receiving total parenteral nutrition (TPN) solution (28% glucose, 4.25% amino acids; 307 kcal/kg/day) enterally (ORAL-TPN) or parenterally (IV-TPN) with or without enteral bulk fiber supplementation. Chow-fed rats served as control subjects. Results The incidence of bacterial translocation in the ORAL-TPN and IV-TPN groups was reduced significantly by the provision of fiber (p < 0.05). Mucosal protein, slgA, and insoluble mucin levels were decreased in the jejunum of the ORAL-TPN and IV-TPN groups, with mucosal protein levels being decreased to a greater extent than slgA or mucin. Although similar decreases in these parameters were observed in the fiber-led groups, fiber appeared to improve intestinal barrier function as measured by horseradish peroxidase permeability. Conclusions The provision of bulk-forming fiber improves intestinal barrier function as measured by peroxidase permeability and bacterial translocation, but does not restore mucosal protein content, intestinal mucin, or slgA levels to normal." @default.
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- W2034160802 date "1994-12-01" @default.
- W2034160802 modified "2023-09-26" @default.
- W2034160802 title "Secretory Immunoglobulin A, Intestinal Mucin, and Mucosal Permeability in Nutritionally Induced Bacterial Translocation in Rats" @default.
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- W2034160802 doi "https://doi.org/10.1097/00000658-199412000-00014" @default.
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