Mice lacking the oxalate transporter SLC26A6 develop hyperoxalemia, hyperoxaluria, and
calcium-oxalate stones as a result of a defect in intestinal oxalate secretion, but what
accounts for the absorptive oxalate flux remains unknown. We measured transepithelial
absorption of [14 C] oxalate simultaneously with the flux of [3 H] mannitol, a marker of the
paracellular pathway, across intestine from wild-type and Slc26a6-null mice. We used the
anion transport inhibitor DIDS to investigate other members of the SLC26 family that may …