Abstract
Derangements in serum phosphate level result in rickets/osteomalacia or ectopic calcification indicating that healthy people without these abnormalities maintain serum phosphate within certain ranges. These results indicate that there must be a regulatory mechanism of serum phosphate level. Fibroblast growth factor 23 (FGF23) was identified as the last member of FGF family. FGF23 is produced by bone and reduces serum phosphate level by suppressing phosphate reabsorption in proximal tubules and intestinal phosphate absorption through lowering 1,25-dihydroxyvitamin D level. It has been shown that excess and deficient actions of FGF23 result in hypophosphatemic rickets/osteomalacia and hyperphosphatemic tumoral calcinosis, respectively. These results indicate that FGF23 works as a hormone, and several disorders of phosphate metabolism can be viewed as endocrine diseases. It may become possible to treat patients with abnormal phosphate metabolism by pharmacologically modifying the activity of FGF23.
Highlights
It is well known that serum calcium (Ca) level is regulated within a narrow range by actions of two calciumregulating hormones, parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25(OH)2D]
It has been known that there are several kinds of hypophosphatemic rickets/osteomalacia with very similar clinical features [16]. These include autosomal dominant and recessive hypophosphatemic rickets/osteomalacia (ADHR, ARHR), X-linked hypophosphatemic rickets/osteomalacia (XLH), hypophosphatemic rickets/osteomalacia associated with McCune-Albright syndrome (MAS)/fibrous dysplasia (FD), and tumor-induced rickets/osteomalacia (TIO)
Serum fibroblast growth factor 23 (FGF23) levels in Hyp mice are elevated, and excess production of FGF23 is found in bone of Hyp mice. These results indicate that the overexpression of FGF23 in bone is responsible for hypophosphatemic rickets/osteomalacia in patients with XLH and Hyp mice
Summary
It is well known that serum calcium (Ca) level is regulated within a narrow range by actions of two calciumregulating hormones, parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25(OH)2D]. While derangements in serum phosphate level result in rickets/osteomalacia or ectopic calcification, the regulatory mechanisms of serum phosphate have been largely unknown. Because PTH and 1,25(OH)2D can affect serum phosphate level, it has been unclear whether there is a tight mechanism of serum phosphate level regulated by a specific phosphateregulating hormone. The identification of fibroblast growth factor 23 (FGF23) and subsequent studies certainly changed this view. FGF23 works as a phosphate-regulating hormone and aberrant functions of FGF23 result in several diseases. We briefly review the physiological and pathophysiological roles of FGF23
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