Importance of anaerobic bacteria in the cobalamin malabsorption of the experimental rat blind loop syndrome

Abstract

Cobalamin malabsorption is a frequent occurrence in the stasis syndrome. Although the exact mechanism for the cobalamin malabsorption has not yet been definied, present evidence supports the avid uptake of cabalamin and to a lesser degree, the intrinsic factor-cobalamin complex by intestinal bacteria. However, correlation between quantitative cultures of the total overgrowth flora and in vivo as well as in vitro parameters of cobalamin absorption has not been fully evaluated. Self-filling blind loops were constructed and the urinary excretion of labeled cyanacobalamin evaluated via metabolic cages which allowed strict separation of urine from feces. Blind loop rats manifested 2.4 ± 1.4% excretion vs. 9.5 ± 1.2% in nonoperated controls, p < 0.001. In other blind loop rats, antibiotic therapy (penicillin, kanamycin, or metronidazole) to selectively suppress bacterial growth was initiated. Penicillin and kanamycin which greatly decreased aerobic grampositive and aerobic gram-negative bacteria, respectively, did not improve cobalamin absorption. However, metronidazole, which markedly decreased anaerobic bacterial growth, corrected cobalamin malabsorption. In vitro studies with bacteria isolated from the small intestine of blind loop rats demonstrated that although aerobic gram-negative bacteria could take up unbound cobalamin, attachment of cobalamin to intrinsic factor greatly reduced the cobalamin uptake. In contrast, intrinsic factor did not protect against extensive binding of cobalamin by anaerobic gram-negative organisms. Bacteroides bound 80.8 ± 8.0% of free cobalamin and 72.1 ± 4.9% of intrinsic factor-cobalamin complex. Thus, anaerobic bacteria, particularly Bacteroides, appear to have a major role in the cobalamin malabsorption of the experimental stasis syndrome.