How do we sense phosphate to regulate serum phosphate level?


Journal

Journal of bone and mineral metabolism
ISSN: 1435-5604
Titre abrégé: J Bone Miner Metab
Pays: Japan
ID NLM: 9436705

Informations de publication

Date de publication:
Jan 2020
Historique:
received: 12 07 2019
accepted: 05 11 2019
pubmed: 5 12 2019
medline: 13 3 2020
entrez: 5 12 2019
Statut: ppublish

Résumé

Abnormal phosphate levels result in several pathological conditions such as rickets/osteomalacia and ectopic calcification indicating that there must be a system that regulates phosphate level within a narrow range. FGF23 has been shown to be an essential hormone regulating serum phosphate level. FGF23 binds to Klotho-FGF receptor complex to reduce serum phosphate level. Several reports suggested that FGF receptor is involved in the regulation of FGF23 production. It has been also shown that high extracellular phosphate can activate several intracellular signaling pathways. However, it has been unclear whether and how phosphate regulates FGF23 production in vivo. Our recent results indicate that high extracellular phosphate directly activates FGF receptor 1 and the downstream intracellular signaling enhances FGF23 production. Thus, there is a negative feedback system for the regulation of serum phosphate level involving FGF receptor and FGF23. We propose that FGF receptor works at least as one of phosphate sensors in the maintenance of serum phosphate level.

Identifiants

pubmed: 31797064
doi: 10.1007/s00774-019-01066-0
pii: 10.1007/s00774-019-01066-0
doi:

Substances chimiques

FGF23 protein, human 0
Phosphates 0
Fibroblast Growth Factors 62031-54-3
Fibroblast Growth Factor-23 7Q7P4S7RRE

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-6

Subventions

Organisme : Japan Society for the Promotion of Science
ID : 19H03676

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Auteurs

Seiji Fukumoto (S)

Department of Molecular Endocrinology, Fujii Memorial Institute of Medical Sciences, Institute of Advanced Medical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8503, Japan. fukumoto-tky@umin.ac.jp.

Yuichi Takashi (Y)

Department of Molecular Endocrinology, Fujii Memorial Institute of Medical Sciences, Institute of Advanced Medical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8503, Japan.
Department of Endocrinology and Diabetes Mellitus, Fukuoka University Chikushi Hospital, 1-1-1 Zokumyoin, Chikushino, 818-8502, Japan.

Maria K Tsoumpra (MK)

Department of Molecular Endocrinology, Fujii Memorial Institute of Medical Sciences, Institute of Advanced Medical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8503, Japan.
Department of Molecular Therapy, National Institute of Neuroscience, National Center for Neurology and Psychiatry, 4-1-1 Ogawahigashi-cho, Kodaira, Tokyo, 187-8502, Japan.

Shun Sawatsubashi (S)

Department of Molecular Endocrinology, Fujii Memorial Institute of Medical Sciences, Institute of Advanced Medical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8503, Japan.

Toshio Matsumoto (T)

Department of Molecular Endocrinology, Fujii Memorial Institute of Medical Sciences, Institute of Advanced Medical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8503, Japan.

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Classifications MeSH