ArticleAmerican journal of physiology. Cell physiology2012
Sat1 is dispensable for active oxalate secretion in mouse duodenum.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Contributions of the anion exchangers SLC26A1, SLC26A2, SLC26A3, and SLC26A6 to intestinal oxalate transport in human Caco2-BBE cells.Physiological reports · 2026Article
- Autophagy Regulates Putative Anion Transporter 1 Expression in Intestinal Epithelial Cells.Journal of cellular and molecular medicine · 2025Article
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- Oxalate homeostasis.Nature reviews. Nephrology · 2023Review
- SLC26A1 is a major determinant of sulfate homeostasis in humans.The Journal of clinical investigation · 2023Article
- SLC26 family: a new insight for kidney stone disease.Frontiers in physiology · 2023Review
- The anion exchanger PAT-1 (Slc26a6) does not participate in oxalate or chloride transport by mouse large intestine.Pflugers Archiv : European journal of physiology · 2021Article
- Enteric Oxalate Secretion Mediated by Slc26a6 Defends against Hyperoxalemia in Murine Models of Chronic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2020Article
- Activation of the PKA signaling pathway stimulates oxalate transport by human intestinal Caco2-BBE cells.American journal of physiology. Cell physiology · 2020Article
- Induction of enteric oxalate secretion by Oxalobacter formigenes in mice does not require the presence of either apical oxalate transport proteins Slc26A3 or Slc26A6.Urolithiasis · 2020Article
- Absence of the sulfate transporter SAT-1 has no impact on oxalate handling by mouse intestine and does not cause hyperoxaluria or hyperoxalemia.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- The role of intestinal oxalate transport in hyperoxaluria and the formation of kidney stones in animals and man.Urolithiasis · 2017Review
- Loss of Cystic Fibrosis Transmembrane Regulator Impairs Intestinal Oxalate Secretion.Journal of the American Society of Nephrology : JASN · 2017Article
- Extracellular Cl(-) regulates human SO4 (2-)/anion exchanger SLC26A1 by altering pH sensitivity of anion transport.Pflugers Archiv : European journal of physiology · 2016Article
- An update on the role of the inflammasomes in the pathogenesis of kidney diseases.Pediatric nephrology (Berlin, Germany) · 2016Review
- In female rats, ethylene glycol treatment elevates protein expression of hepatic and renal oxalate transporter sat-1 (Slc26a1) without inducing hyperoxaluria.Croatian medical journal · 2015Article
- NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy.Kidney international · 2013Article
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5 authors at 2 institutions in 2 countries.
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Abstract
Mice deficient for the apical membrane oxalate transporter SLC26A6 develop hyperoxalemia, hyperoxaluria, and calcium oxalate stones due to a defect in intestinal oxalate secretion. However, the nature of the basolateral membrane oxalate transport process that operates in series with SLC26A6 to mediate active oxalate secretion in the intestine remains unknown. Sulfate anion transporter-1 (Sat1 or SLC26A1) is a basolateral membrane anion exchanger that mediates intestinal oxalate transport. Moreover, Sat1-deficient mice also have a phenotype of hyperoxalemia, hyperoxaluria, and calcium oxalate stones. We, therefore, tested the role of Sat1 in mouse duodenum, a tissue with Sat1 expression and SLC26A6-dependent oxalate secretion. Although the active secretory flux of oxalate across mouse duodenum was strongly inhibited (>90%) by addition of the disulfonic stilbene DIDS to the basolateral solution, secretion was unaffected by changes in medium concentrations of sulfate and bicarbonate, key substrates for Sat1-mediated anion exchange. Inhibition of intracellular bicarbonate production by acetazolamide and complete removal of bicarbonate from the buffer also produced no change in oxalate secretion. Finally, active oxalate secretion was not reduced in Sat1-null mice. We conclude that a DIDS-sensitive basolateral transporter is involved in mediating oxalate secretion across mouse duodenum, but Sat1 itself is dispensable for this process.
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