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2014 ; 592
(18
): 3985-95
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Regulation of serum phosphate
#MMPMID24973411
Lederer E
J Physiol
2014[Sep]; 592
(18
): 3985-95
PMID24973411
show ga
The regulation of serum phosphate, an acknowledged risk factor for chronic kidney
disease and cardiovascular mortality, is poorly understood. The discovery of
fibroblast growth factor 23 (FGF23) as a key regulator of renal phosphate
handling and activation of vitamin D has revolutionized our comprehension of
phosphate homeostasis. Through as yet undetermined mechanisms, circulating and
dietary phosphate appear to have a direct effect on FGF23 release by bone cells
that, in turn, causes renal phosphate excretion and decreases intestinal
phosphate absorption through a decrease in vitamin D production. Thus, the two
major phosphaturic hormones, PTH and FGF23, have opposing effects on vitamin D
production, placing vitamin D at the nexus of phosphate homeostasis. While our
understanding of phosphate homeostasis has advanced, the factors determining
regulation of serum phosphate level remain enigmatic. Diet, time of day, season,
gender, age and genetics have all been identified as significant contributors to
serum phosphate level. The effects of these factors on serum phosphate have major
implications for what is understood as 'normal' and for studies of phosphate
homeostasis and metabolism. Moreover, other hormonal mediators such as dopamine,
insulin-like growth factor, and angiotensin II also affect renal handling of
phosphate. How the major hormone effects on phosphate handling are regulated and
how the effect of these other factors are integrated to yield the measurable
serum phosphate are only now beginning to be studied.
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