Phosphorus: Another Devil in Our Diet? Yeong-Hau H. Lien, MD, PhD  The American Journal of Medicine  Volume 126, Issue 4, Pages 280-281 (April 2013) DOI: 10.1016/j.amjmed.2012.10.019 Copyright © 2013 Elsevier Inc. Terms and Conditions

Figure Regulation of phosphorus homeostasis: In response to high phosphorus intake, parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) are released from parathyroid gland and bone, respectively. The release of PTH can be abolished by simultaneous high calcium intake.8 Both PTH and FGF23 suppress renal sodium phosphate cotransporter-2a (NaPi-2a) and NaPi-2c activities to increase the urinary excretion of phosphorus. FGF23 also suppresses renal expression of 1-α-hydroxylase (1α[OH]ase) to reduce production of 1,25-dihydroxy vitamin D (1,25[OH]2D). As a result, intestinal NaPi-2b activities are reduced, and subsequently, less phosphorus is absorbed. The increased urinary excretion and decreased intestinal absorption therefore lower serum phosphorus levels. The FGF23 action requires Klotho, which is an essential cofactor for the interaction between FGF23 and FGF receptor. The American Journal of Medicine 2013 126, 280-281DOI: (10.1016/j.amjmed.2012.10.019) Copyright © 2013 Elsevier Inc. Terms and Conditions