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2017 ; 7
(1
): 11018
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English Wikipedia
The intestinal phosphate transporter NaPi-IIb (Slc34a2) is required to protect
bone during dietary phosphate restriction
#MMPMID28887454
Knöpfel T
; Pastor-Arroyo EM
; Schnitzbauer U
; Kratschmar DV
; Odermatt A
; Pellegrini G
; Hernando N
; Wagner CA
Sci Rep
2017[Sep]; 7
(1
): 11018
PMID28887454
show ga
NaPi-IIb/Slc34a2 is a Na(+)-dependent phosphate transporter that accounts for the
majority of active phosphate transport into intestinal epithelial cells. Its
abundance is regulated by dietary phosphate, being high during dietary phosphate
restriction. Intestinal ablation of NaPi-IIb in mice leads to increased fecal
excretion of phosphate, which is compensated by enhanced renal reabsorption. Here
we compared the adaptation to dietary phosphate of wild type (WT) and
NaPi-IIb(-/-) mice. High phosphate diet (HPD) increased fecal and urinary
excretion of phosphate in both groups, though NaPi-IIb(-/-) mice still showed
lower urinary excretion than WT. In both genotypes low dietary phosphate (LDP)
resulted in reduced fecal excretion and almost undetectable urinary excretion of
phosphate. Consistently, the expression of renal cotransporters after prolonged
LDP was similar in both groups. Plasma phosphate declined more rapidly in
NaPi-IIb(-/-) mice upon LDP, though both genotypes had comparable levels of
1,25(OH)(2)vitamin D(3), parathyroid hormone and fibroblast growth factor 23.
Instead, NaPi-IIb(-/-) mice fed LDP had exacerbated hypercalciuria, higher
urinary excretion of corticosterone and deoxypyridinoline, lower bone mineral
density and higher number of osteoclasts. These data suggest that during dietary
phosphate restriction NaPi-IIb-mediated intestinal absorption prevents excessive
demineralization of bone as an alternative source of phosphate.