Affiliations: Department of Clinical Nutrition, Institute of Health
Biosciences, University of Tokushima Graduate School, Tokushima, Japan
Note: [] Address for correspondence: Eiji Takeda, M.D., Ph.D., Department
of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima
Graduate School, Kuramoto-cho 3-18-15, Tokushima, 770-8503, Japan. Tel.: +81 88
633 7093; Fax: +81 88 633 7094; E-mail: [email protected]
Abstract: Inorganic phosphate (Pi) is required for cellular function and
skeletal mineralization. Serum Pi level is maintained within a narrow range
through a complex interplay between intestinal absorption, exchange with
intracellular and bone storage pools, and renal tubular reabsorption. Pi is
abundant in the diet, and intestinal absorption of Pi is efficient and
minimally regulated. The kidney is a major regulator of Pi homeostasis and can
increase or decrease its Pi reabsorptive capacity to accommodate Pi need. The
crucial regulated step in Pi homeostasis is the transport of Pi across the
renal proximal tubule. Type II sodium-dependent phosphate (Na/Pi) cotransporter
(NPT2) is the major molecule in the renal proximal tubule and is regulated by
hormones and nonhormonal factors. Recent studies of inherited and acquired hypophosphatemia which
exhibit similar biochemical and clinical features, have led to the
identification of novel genes, phosphate regulating gene with homologies to
endopeptidases on the X chromosome (PHEX) and fibroblast growth factor-23
(FGF-23), that play a role in the regulation of Pi homeostasis. The PHEX gene
encodes an endopeptidase, predominantly expressed in bone and teeth but not in
kidney. FGF-23 may be a substrate of this endopeptidase and inhibit renal Pi
reabsorption. In a survey in the United States and in Japan, the amount of
phosphorus from food is gradually increasing. It is thought that excess amounts
of phosphorus intake for long periods are a strong factor in bone impairment
and ageing. The restriction of phosphorus intake seems to be important under
low calcium intake to keep QOL on high level.
