Physiological roles of mammalian sulfate transporters NaS1 and Sat1
D Markovich - Archivum immunologiae et therapiae experimentalis, 2011 - Springer
D Markovich
Archivum immunologiae et therapiae experimentalis, 2011•SpringerThis review summarizes the physiological roles of the renal sulfate transporters NaS1
(Slc13a1) and Sat1 (Slc26a1). NaS1 and Sat1 encode renal anion transporters that mediate
proximal tubular sulfate reabsorption and thereby regulate blood sulfate levels. Targeted
disruption of murine NaS1 and Sat1 leads to hyposulfatemia and hypersulfaturia. Sat1 null
mice also exhibit hyperoxalemia, hyperoxaluria and calcium oxalate urolithiasis.
Dysregulation of NaS1 and Sat1 leads to hypersulfaturia, hyposulfatemia and liver damage …
(Slc13a1) and Sat1 (Slc26a1). NaS1 and Sat1 encode renal anion transporters that mediate
proximal tubular sulfate reabsorption and thereby regulate blood sulfate levels. Targeted
disruption of murine NaS1 and Sat1 leads to hyposulfatemia and hypersulfaturia. Sat1 null
mice also exhibit hyperoxalemia, hyperoxaluria and calcium oxalate urolithiasis.
Dysregulation of NaS1 and Sat1 leads to hypersulfaturia, hyposulfatemia and liver damage …
Abstract
This review summarizes the physiological roles of the renal sulfate transporters NaS1 (Slc13a1) and Sat1 (Slc26a1). NaS1 and Sat1 encode renal anion transporters that mediate proximal tubular sulfate reabsorption and thereby regulate blood sulfate levels. Targeted disruption of murine NaS1 and Sat1 leads to hyposulfatemia and hypersulfaturia. Sat1 null mice also exhibit hyperoxalemia, hyperoxaluria and calcium oxalate urolithiasis. Dysregulation of NaS1 and Sat1 leads to hypersulfaturia, hyposulfatemia and liver damage. Loss of Sat1 leads additionally to hyperoxaluria with hyperoxalemia, nephrocalcinosis and calcium oxalate urolithiasis. These data indicate that the renal anion transporters NaS1 and Sat1 are essential for sulfate and oxalate homeostasis, respectively.
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