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Elevated FGF23 Levels in Mice Lacking the Thiazide-Sensitive NaCl cotransporter (NCC)
Ganesh Pathare1,2,3, Manuel Anderegg4,5,6, Giuseppe Albano4,5,6
1Division of Nephrology and Hypertension, Bern University Hospital, University of Bern, Bern, Switzerland. ganesh.pathare@ibmm.unibe.ch.
Scientific Reports
|February 28, 2018
Summary
Lack of the thiazide-sensitive sodium chloride cotransporter (NCC) increases fibroblast growth factor 23 (FGF23) levels. This FGF23 upregulation is mediated by aldosterone, impacting mineral metabolism.
Area of Science:
- Nephrology
- Endocrinology
- Mineral Metabolism
Background:
- Fibroblast growth factor 23 (FGF23) regulates phosphate and vitamin D metabolism.
- FGF23 release is stimulated by aldosterone and extracellular volume depletion.
Purpose of the Study:
- To investigate the role of the thiazide-sensitive sodium chloride cotransporter (NCC) in regulating FGF23 levels.
- To characterize the effect of mild hypovolemia on FGF23 in NCC knockout mice.
Main Methods:
- Comparison of FGF23, PTH, aldosterone, and vitamin D levels between NCC knockout (KO) and wild-type (WT) mice.
- Analysis of renal gene expression for FGF23, its receptor (FGFR1), and co-receptor (Klotho).
- Assessment of mineralocorticoid receptor antagonist (eplerenone) effects on FGF23 levels.
Main Results:
- NCC KO mice exhibited significantly higher FGF23, PTH, and aldosterone concentrations than WT mice.
- 1,25(OH)2D3, fractional phosphate excretion, and renal sodium/phosphate co-transporter 2a expression were similar between genotypes.
- Increased FGF23 transcript in bone of NCC KO mice was reversed by eplerenone, indicating aldosterone mediation.
Conclusions:
- Absence of renal NCC leads to an aldosterone-mediated increase in circulating FGF23.
- This finding highlights a novel link between NCC, aldosterone, and FGF23 regulation in mineral homeostasis.
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