BACKGROUND: Normal gut flora plays an important role in the intestinal mucosal barrier function under various critical conditions. The flora may alter after severe insults, such as trauma and shock. Enteral nutrition should preserve the gut environment; however, full support is usually difficult for severely ill patients because of impaired gastrointestinal motility. Currently, we have commercial enteral supplementation product enriched with glutamine, dietary fiber, and oligosaccharide (GFO) in Japan. This study examines the hypothesis that the enteral supplementation ameliorates gut injury induced by a bacterial overgrowth model, even in small volumes and quantities. MATERIALS: Balb/c mice received antibiotics (4 mg/mL of streptomycin) in their drinking water for 4 days to kill the normal gut flora after which they were orally inoculated with a streptomycin-resistant strain of Escherichia coli, known as E. coli C-25. The mice that were administered bacterial monoassociation received 0.5 mL of GFO twice daily (GFO group) or 10% of glucose solution (GLU group). Unsupplemented drinking water was used for control animals (control) whose gut flora was normal. The mice were killed and their mesenteric lymph nodes complex was harvested and processed to test gut bacterial translocation. The cecal population levels of bacteria and ileum histology were also examined. RESULTS: The incidence and magnitude of gut translocation to the lymph nodes complex in the GLU group were significantly higher than those in the control (p < 0.01). Treatment with GFO prevented the gut translocation although animals in the GFO group had same level of the cecal bacterial population. Histologic findings in the ileum were not different between the GLU and GFO. CONCLUSION: GFOs supplement prevented gut translocation for bacterial overgrowth even in small volumes and quantities. The intestinal histologic findings could not explain the protective mechanisms of GFO. Further studies may be needed to elucidate the benefit of the partial enteral nutrition.
BACKGROUND: Normal gut flora plays an important role in the intestinal mucosal barrier function under various critical conditions. The flora may alter after severe insults, such as trauma and shock. Enteral nutrition should preserve the gut environment; however, full support is usually difficult for severely ill patients because of impaired gastrointestinal motility. Currently, we have commercial enteral supplementation product enriched with glutamine, dietary fiber, and oligosaccharide (GFO) in Japan. This study examines the hypothesis that the enteral supplementation ameliorates gut injury induced by a bacterial overgrowth model, even in small volumes and quantities. MATERIALS: Balb/c mice received antibiotics (4 mg/mL of streptomycin) in their drinking water for 4 days to kill the normal gut flora after which they were orally inoculated with a streptomycin-resistant strain of Escherichia coli, known as E. coli C-25. The mice that were administered bacterial monoassociation received 0.5 mL of GFO twice daily (GFO group) or 10% of glucose solution (GLU group). Unsupplemented drinking water was used for control animals (control) whose gut flora was normal. The mice were killed and their mesenteric lymph nodes complex was harvested and processed to test gut bacterial translocation. The cecal population levels of bacteria and ileum histology were also examined. RESULTS: The incidence and magnitude of gut translocation to the lymph nodes complex in the GLU group were significantly higher than those in the control (p < 0.01). Treatment with GFO prevented the gut translocation although animals in the GFO group had same level of the cecal bacterial population. Histologic findings in the ileum were not different between the GLU and GFO. CONCLUSION:GFOs supplement prevented gut translocation for bacterial overgrowth even in small volumes and quantities. The intestinal histologic findings could not explain the protective mechanisms of GFO. Further studies may be needed to elucidate the benefit of the partial enteral nutrition.