The Role of Sodium-Dependent Phosphate Transporter in Phosphate Homeostasis

Access this Article

Author(s)

    • MIYAMOTO Ken-ichi
    • Department of Molecular Nutrition, Institute of Medical Nutrition, The University of Tokushima School of Medicine

Abstract

Inorganic phosphate (Pi) is an essential compound for several biologic functions. Pi levels outside the normal range, however, contribute to several pathological processes. Hypophosphatemia leads to bone abnormalities, such as rickets/osteomalacia. Hyperphosphatemia contributes to vascular calcification in patients with chronic kidney disease and hemodialysis patients and is independently associated with cardiac mortality.<br>Pi homeostasis is regulated by the coordinated function of renal and intestinal sodium-dependent phosphate (NaPi) transporters with dietary Pi, parathyroid hormone, 1,25-dihydroxyvitamin D<sub>3</sub>, and fibroblast growth factor 23. The type II NaPi transporter/SLC34 family, with three members identified to date, is mainly responsible for Pi homeostasis in the body. SLC34A1 and SCL34A3 are predominantly expressed in the kidney, whereas SLC34A2 is expressed in the small intestine. The role of each SLC34 in the body was recently established by studies of gene-targeted mice. Mutation of SLC34A1 causes Fanconi syndrome and mutation of SLC34A3 causes autosomal recessive hereditary hypophosphatemic rickets with hypercalciuria. SLC34A2 is thought to be a major intestinal NaPi transporter and mutation of SLC34A2 causes pulmonary alveolar microlithiasis. A detailed understanding of Pi regulation in the body is important toward maintaining health.

Journal

  • Journal of Nutritional Science and Vitaminology

    Journal of Nutritional Science and Vitaminology 61(Supplement), S119-S121, 2015

    Center for Academic Publications Japan

Codes

  • NII Article ID (NAID)
    130005109878
  • NII NACSIS-CAT ID (NCID)
    AA00703822
  • Text Lang
    ENG
  • ISSN
    0301-4800
  • NDL Article ID
    026364097
  • NDL Call No.
    Z53-B484
  • Data Source
    NDL  J-STAGE 
Page Top