Abstract
The Fibroblast Growth Factor 23 (FGF23) has been identified less than 20 years ago. It rapidly appeared that FGF23 was not only the hormone that control phosphate homeostasis but also the metabolism of the active form of vitamin D, calcitriol. FGF23, by contrast with many other FGF belongs to the small hormone-like FGF sub-family with FGF15/19 and FGF21. FGF23 is secretes by osteocytes and osteoblasts in response to high phosphate or calcitriol levels. FGF23 inhibits the expression of renal sodium phosphate transporters, which augments phosphate excretion in urine. FGF23 also stimulates the expression of the enzyme that inactivates calcitriol, the CYP24A1, and lowers the expression of CYP27B1, which converts 25(OH) vitamin D into calcitriol. Hence FGF23 controls calcitriol levels in plasma. By decreasing calcitriol levels FGF23 indirectly diminishes intestinal phosphate absorption. Calcitriol directly stimulates FGF23 production in osteocytes. The physiological action of FGF23 requires the expression at the cell surface of a FGFR and the co-receptor αklotho. αKlotho is mainly expressed in the kidney, brain, and in the muscle. Calcitriol stimulates αklotho expression. αKlotho can be released from the cell surface by cleavage producing a circulating protein the role of which is insufficiently delineated, see previous chapter. FGF23 concentration increases at the early steps of renal insufficiency to maintain plasma phosphate concentration within normal range. This participates to the genesis of secondary hyperparathyroidism. High concentrations of FGF23 induce cardiac hypertrophy despite the absence of klotho in cardiac tissue. The decrease in calcitriol concentration induced by FGF23 may contribute to its deleterious effect on heart.
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Prié, D. (2016). Vitamin D and FGF23 in Chronic Kidney Disease. In: Ureña Torres, P., Cozzolino, M., Vervloet, M. (eds) Vitamin D in Chronic Kidney Disease. Springer, Cham. https://doi.org/10.1007/978-3-319-32507-1_10
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DOI: https://doi.org/10.1007/978-3-319-32507-1_10
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