Studies on the pathogenesis of steatorrhea in the blind ioop syndrome

In patients with the blind loop syndrome in-testinal abnormalities conducive to stasis and bac-terial proliferation within the contents of the small bowel are associated with vitamin B12 de-ficiency and steatorrhea (1). Mechanisms in-volved in the pathogenesis of this syndrome have not been defined although evidence derived from patients (2) and experimental animals (3) sug-gests that the host may be deprived of vitamin B12 because bacterial uptake of microgram quan-tities of the vitamin makes it unavailable for absorption. A similar explanation for steatorrhea seems less likely, however, since in the case of lipids, bacteria would have to compete for gram rather than microgram quantities. Reports of steatorrhea in clinical (2, 4, 5) and experimental (6, 7) forms of the blind loop syndrome have demonstrated decreased fecal fat excretion after antibiotic therapy, but such studies have not pro-vided evidence concerned with mechanisms whereby small bowel bacterial overgrowth might result in steatorrhea. Excessive fecal fat losses in the blind loop syn-drome could occur in the absence of malabsorp-tion if intestinal production of lipids derived from intestinal bacteria or from sloughed intestinal mucosal cells were increased. On the other hand, it is entirely possible that intraluminal bacteria might be capable of impairing one or more of the processes normally involved in the absorption of dietary fat. In the present investigation studies were car-ried out in rats with experimentally induced smal