| First Author | Dawson PA | Year | 2003 |
| Journal | Proc Natl Acad Sci U S A | Volume | 100 |
| Issue | 23 | Pages | 13704-9 |
| PubMed ID | 14578452 | Mgi Jnum | J:86561 |
| Mgi Id | MGI:2680764 | Doi | 10.1073/pnas.2231298100 |
| Citation | Dawson PA, et al. (2003) Hyposulfatemia, growth retardation, reduced fertility, and seizures in mice lacking a functional NaSi-1 gene. Proc Natl Acad Sci U S A 100(23):13704-9 |
| abstractText | Inorganic sulfate is required for numerous functions in mammalian physiology, and its circulating levels are proposed to be maintained by the Na+-SO42- cotransporter, (NaSi-1). To determine the role of NaSi-1 in sulfate homeostasis and the physiological consequences in its absence, we have generated a mouse lacking a functional NaSi-1 gene, Nas1. Serum sulfate concentration was reduced by >75% in Nas1-/- mice when compared with Nas1+/+ mice. Nas1-/- mice exhibit increased urinary sulfate excretion, reduced renal and intestinal Na+-SO42- cotransport, and a general growth retardation. Nas1-/- mouse body weight was reduced by >20% when compared with Nas1+/+ and Nas1+/- littermates at 2 weeks of age and remained so throughout adulthood. Nas1-/- females had a lowered fertility, with a 60% reduction in litter size. Spontaneous clonic seizures were observed in Nas1-/- mice from 8 months of age. These data demonstrate NaSi-1 is essential for maintaining sulfate homeostasis, and its expression is necessary for a wide range of physiological functions. |
