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Absence of the sulfate transporter SAT-1 (Slc26a1) has no impact on oxalate handling by mouse intestine and does not cause hyperoxaluria or hyperoxalemia.

The anion exchanger SAT-1 (Sulfate Anion Transporter 1; Slc26a1), is considered an important regulator of oxalate and sulfate homeostasis but the mechanistic basis of these critical roles remain undetermined. Previously, characterization of the SAT-1 knockout (KO) mouse suggested the loss of SAT-1 mediated oxalate secretion by the intestine was responsible for the hyperoxaluria, hyperoxalemia and calcium oxalate urolithiasis reportedly displayed by this model. To test this hypothesis, we compared the transepithelial fluxes of 14 C-oxalate, 35 SO4 2- and 36 Cl- across isolated, short-circuited segments of the distal ileum, cecum and distal colon from wild-type (WT) and SAT-1 KO mice. The absence of SAT-1 did not impact the transport of these anions by any part of the intestine examined. Additionally, SAT-1 KO mice were neither hyperoxaluric nor hyperoxalemic. Instead, 24-hour urinary oxalate excretion was almost 50 % lower than WT mice. With no contribution from the intestine, we suggest this may reflect the loss of SAT-1 mediated oxalate efflux from the liver. SAT-1 KO mice were, however, profoundly hyposulfatemic even though there were no changes to intestinal sulfate handling and the renal clearances of sulfate and creatinine indicated diminished rates of sulfate re-absorption by the proximal tubule. Aside from this distinct sulfate phenotype we were unable to reproduce the hyperoxaluria, hyperoxalemia and urolithiasis of the original SAT-1 KO model. In conclusion, oxalate and sulfate transport by the intestine was not dependent on SAT-1 and we found no evidence supporting the long-standing hypothesis that intestinal SAT-1 contributes to oxalate and sulfate homeostasis.

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