Effects of Dietary Iron Intake and Chronic Kidney Disease on Fibroblast Growth Factor 23 Metabolism in Wild Type and Hepcidin Knockout Mice.

Effects of Dietary Iron Intake and Chronic Kidney Disease on Fibroblast Growth Factor 23 Metabolism in Wild Type and Hepcidin Knockout Mice. Am J Physiol Renal Physiol. 2016 Oct 12;:ajprenal.00281.2016 Authors: Hanudel MR, Chua K, Rappaport M, Gabayan V, Valore E, Goltzman D, Ganz T, Nemeth E, Salusky IB Abstract In the setting of normal kidney function, iron deficiency is associated with increased FGF23 production and cleavage, altering circulating FGF23 levels. Our objective was to determine how chronic kidney disease (CKD) and dietary iron intake affect FGF23 production and metabolism in wild type (WT) and hepcidin knockout (HKO) mice. For eight weeks, the mice were fed diets that contained adenine (to induce CKD) or no adenine (control group), with either low iron (4 ppm) or standard iron (335 ppm) concentrations. The low iron diet induced iron deficiency anemia in both the WT and HKO mice. Among the WT mice, in both the control and CKD groups, low iron compared to standard iron diet increased bone Fgf23 mRNA expression, C-terminal FGF23 (cFGF23) levels, and FGF23 cleavage as manifested by a lower percentage intact FGF23 (iFGF23). Independent of iron status, CKD was associated with inhibition of FGF23 cleavage. Similar results were observed in the HKO control and CKD groups. Dietary iron content was more influential on FGF23 parameters than the presence or absence of hepcidin. In the CKD mice (WT and HKO, total n=42), independent...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research