Abstract
Background: In order to understand the consequences of persistent enteral feeding in patients with carbohydrate malabsorption, we fed piglets lactulose in sufficient dosage to produce osmotic diarrhea or inulin, using a conventional dose, to determine if this prebiotic can modulate the effects of lactulose. Feeding lactulose increases cecal luminal synthesis of butyrate, with inulin having an intermediate effect. Because clostridia may be a major source of colonic butyrate production, we hypothesized that feeding piglets lactulose or inulin would increase cecal densities of clostridia. Methods: Piglets were assigned to 3 formula study groups for 6 days: (1) control, fed only sow milk replacer (n = 12); (2) inulin, inulin supplement (3 g/L; n = 11); and (3) lactulose, lactulose supplement (66.7 g/L; n = 6). Cecal fluid for bacteriological studies was sampled intraoperatively. Results: The wet/dry ratio of the cecal contents (mean ± SEM) was 8.2 ± 0.5, 6.2 ± 0.5, and 18.8 ± 5.5, respectively, in the control, inulin, and lactulose groups (p = .049, Kruskal-Wallis). There were no differences among the diet groups for cecal densities (106 colony-forming units [CFU]/g dry wt cecal contents) of total anaerobes, total aerobes, bifidobacteria, or lactobacilli. Densities of clostridia were markedly reduced in the lactulose group (1.14 ± 0.41) vs the control (18.39 ± 4.44; p = .001) or inulin groups (8.87 ± 2.20; p = .04). Conclusions: In piglets, feeding lactulose at a dose known to cause diarrhea reduces cecal densities of clostridia.
Feeding an indigestible, fructose-containing disaccharide (lactulose) to piglets caused a marked reduction in the cecal density of clostridial species. These results may have relevance to the prevention of necrotizing enterocolitis or to biochemical mechanisms explaining how fructooligosaccharides alter gut cell kinetics.
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