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Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Sciences.
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2003 In: Kidney Int, ISSN 0085-2538, Vol. 6, no 64, 2272-9 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2003. Vol. 6, no 64, 2272-9 p.
Identifiers
URN: urn:nbn:se:uu:diva-91996OAI: oai:DiVA.org:uu-91996DiVA: diva2:164927
Available from: 2004-09-02 Created: 2004-09-02Bibliographically approved
In thesis
1. The Role of Fibroblast Growth Factor 23 in Phosphate Homeostasis
Open this publication in new window or tab >>The Role of Fibroblast Growth Factor 23 in Phosphate Homeostasis
2004 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The regulation of serum phosphate (Pi) concentrations is a complex process and our current models are far from complete. Due to major advancements in biotechnology and the development of more powerful research tools, recent advances in the field of genetics has led to the identification of several candidates for the long sought-after phosphatonin(s), or Pi regulating hormones. One of these candidates is fibroblast growth factor 23 (FGF-23) and this thesis is based upon studies of the role of FGF-23 in Pi homeostasis. We demonstrate that FGF-23 is a secreted protein which is highly expressed in tumors giving rise to oncogenic hypophosphatemic osteomalacia (OOM). Furthermore, we have developed a two-site enzyme-linked immunosorbent assay for the detection of circulating FGF-23 and established that FGF-23 is present in the circulation of healthy individuals. Also, FGF-23 serum levels are elevated in patients with disturbances in Pi homeostasis such as OOM, X-linked hypophosphatemic rickets (XLH) and chronic kidney disease and are likely to play an important role in the pathogenesis of these disorders. A transgenic mouse model that express human FGF-23 under the control of the α1(I) collagen promoter exhibit similar clinical and biochemical characteristics as do patients with OOM, XLH and autosomal dominant hypophosphatemic rickets indicating that FGF-23 is an important determinant of Pi homeostasis, vitamin D metabolism and bone mineralization.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2004. 78 p.
Series
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1367
Keyword
Medicine, Fibroblast Growth Factor 23, FGF-23, phosphate homeostasis, vitamin D metabolism, sodium/phosphate cotransporters, autosomal dominant hypophosphatemic rickets, ADHR, X-linked hypophosphatemic rickets, XLH, oncogenic osteomalacia, OOM, PHEX, Medicin
National Category
Dermatology and Venereal Diseases
Identifiers
urn:nbn:se:uu:diva-4489 (URN)91-554-6013-5 (ISBN)
Public defence
2004-09-25, Enghoffsalen, UAS, ingång 50, b.v, Uppsala, 13:15
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Supervisors
Available from: 2004-09-02 Created: 2004-09-02 Last updated: 2013-12-05Bibliographically approved

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