Moreover, the induction of functional iron deficiency without superimposed inflammation was produced by administration of exogenous hepcidin into wild-type mice, where bone expression and C-terminal FGF23 levels were significantly elevated as a result of the stabilization of hypoxia-inducible factor 1α (HIF1α) and its subsequent translocation and binding to hypoxia response elements on the Fgf23 promoter [179]. Here, FGF23 is linked to nutritional disorder.