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First published online on February 7, 2006
Endocrine Reviews, doi:10.1210/er.2005-0019
A more recent version of this article appeared on May 1, 2006
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*Endocrine Diseases

The Roles of Specific Genes Implicated as Circulating Factors Involved in Normal and Disordered Phosphate Homeostasis: Frp-4, MEPE, and FGF23

Kenneth E. White, Tobias M. Larsson, and Michael J. Econs*

Department of Medical and Molecular Genetics, and Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, 46202 USA

* To whom correspondence should be addressed. E-mail: mecons{at}iupui.edu.

Normal serum phosphate (Pi) concentrations are relatively tightly controlled by endocrine mediators of Pi balance. Recent data involving several disorders of Pi homeostasis have shed new light on the regulation of serum Pi balance. It has been hypothesized that circulating phosphaturic factors, or ‘phosphatonins’, exist that, when present at high serum concentrations, directly act on the kidney to induce renal Pi wasting. This review will focus upon recently discovered factors that are over expressed in tumors associated with tumor induced osteomalacia, and have reported activity consistent with effecting Pi balance in vivo. Currently, the best-characterized group of phosphatonin-like polypeptides includes secreted frizzled related protein-4 (FRP4), matrix extracellular phosphoglycoprotein (MEPE), and fibroblast growth factor-23 (FGF23). Our understanding of these factors will in the short term, aid us in understanding normal Pi balance, and in the future, help to design novel therapeutic strategies for disorders of Pi handling.
Key words: FRP4 • MEPE • FGF • FGF23 • FGF-23 • metabolic bone disease • ADHR • TIO • XLH • fibrous dysplasia • phosphate • Pi wasting




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