Journal
BONE
Volume 45, Issue -, Pages S2-S7Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bone.2009.02.003
Keywords
SLC34; Renal phosphate transporter; Hypophosphatemia; Rickets; Kidney; Bone
Categories
Funding
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [19790585, 11557202]
- Grants-in-Aid for Scientific Research [19790585, 11557202] Funding Source: KAKEN
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The renal type II Na/Pi cotransporters, Na/Pi-IIa and Na/Pi-IIc, are expressed in the brush border membrane (BBM) of the renal proximal tubule cells. Because it has long been thought that Na/Pi-IIa alone can regulate the reabsorption of phosphate in the proximal renal tubules, Na/Pi-IIc has not been paid much attention by the renal research community. Recent studies, however, have identified Na/Pi-IIc mutations as the defective cause of hereditary hypophosphatemic rickets with hypercalciuria (HHRH). This finding indicates that Na/Pi-IIc has a rather important role in renal Pi reabsorption and bone mineralization, and that it may be a key determinant of plasma Pi concentrations in humans. Studies of Na/Pi-IIc mice indicate that Na/Pi-IIc is necessary for normal calcium homeostasis, but its role in the regulation Of Pi metabolism and bone physiology may be different from that in HHRH patients. Of note, Na/Pi-IIc KO mice display abnormal vitamin D regulation Without hypophosphatemia or hyperphosphaturia. Thus, Na/Pi-IIc may be involved in regulating renal vitamin D synthesis in the proximal tubular cells. The identification Of proteins that interact with Na/Pi-IIc is an important area of future research. The physiologic roles of Na/Pi-IIa and Na/Pi-IIc require future elucidation. (c) 2009 Elsevier Inc. All rights reserved.
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