Enteric oxalate elimination is induced and oxalate is normalized in a mouse model of primary hyperoxaluria following intestinal colonization with Oxalobacter.

[primary hyperoxaluria type 1]

Oxalobacter colonization of rat intestine was previously shown to promote enteric oxalate secretion and elimination , leading to significant reductions in urinary oxalate excretion (Hatch et al . Kidney Int 69 : 691 -698 , 2006 ). The main goal of the present study , using a mouse model of primary hyperoxaluria type 1 (PH 1 ), was to test the hypothesis that colonization of the mouse gut by Oxalobacter formigenes could enhance enteric oxalate secretion and effectively reduce the hyperoxaluria associated with this genetic disease . Wild-type (WT ) mice and mice deficient in liver alanine-glyoxylate aminotransferase (Agxt ) exhibiting hyperoxalemia and hyperoxaluria were used in these studies . We compared the unidirectional and net fluxes of oxalate across isolated , short -circuited large intestine of artificially colonized and noncolonized mice . In addition , plasma and urinary oxalate was determined . Our results demonstrate that the cecum and distal colon contribute significantly to enteric oxalate excretion in Oxalobacter-colonized Agxt and WT mice . In colonized Agxt mice , urinary oxalate excretion was reduced 50 % (to within the normal range observed for WT mice ). Moreover , plasma oxalate concentrations in Agxt mice were also normalized (reduced 50 %). Colonization of WT mice was also associated with marked (up to 95 %) reductions in urinary oxalate excretion . We conclude that segment-specific effects of Oxalobacter on intestinal oxalate transport in the PH 1 mouse model are associated with a normalization of plasma oxalate and urinary oxalate excretion in otherwise hyperoxalemic and hyperoxaluric animals .

Diseases
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Diseases presenting "specific effects" symptom

cushing syndrome

familial hypocalciuric hypercalcemia

primary hyperoxaluria type 1

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