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Regulatory mechanisms of circulating fibroblast growth factor 23 in parathyroid diseases.
Ther Apher Dial. 2007 Oct; 11 Suppl 1:S32-7.TA

Abstract

Fibroblast growth factor-23 (FGF-23) is a circulating factor regulating phosphate and vitamin D homeostasis. Phosphate intake and an administration of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) increase circulating FGF-23 levels, and elevated FGF-23 prevents hyperphosphatemia and vitamin D toxicity by hyperphosphaturia and suppression of circulating 1,25(OH)(2)D level, comprising a feedback loop to maintain phosphate and vitamin D homeostasis. Excess secretion of parathyroid hormone (PTH), another phosphaturic factor, elevates the serum calcium level in primary hyperparathyroidism. PTH also elevates circulating FGF-23 level, which cooperatively enhances the phosphaturia, resulting in hypophosphatemia. The circulating FGF-23 level increases as renal function declines in chronic kidney disease (CKD), and it exhibits significant and positive correlations with serum phosphate, calcium, and PTH in CKD patients on maintenance hemodialysis, suggesting that these parameters regulate circulating FGF-23 level. Tight associations between circulating FGF-23 and calcium levels were observed both in patients with primary hyperparathyroidism and in CKD patients on maintenance hemodialysis, suggesting the role of serum calcium on FGF-23 regulatory mechanisms. FGF-23 may have a physiological role in preventing tissue damage such as ectopic calcifications, partly via suppressing the serum calcium x phosphate product by accelerating urinary phosphate excretion and suppressing vitamin D activation.

Authors+Show Affiliations

Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, Abeno-ku, Osaka, Japan. imanishi@med.osaka-cu.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

17976083

Citation

Imanishi, Yasuo, et al. "Regulatory Mechanisms of Circulating Fibroblast Growth Factor 23 in Parathyroid Diseases." Therapeutic Apheresis and Dialysis : Official Peer-reviewed Journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy, vol. 11 Suppl 1, 2007, pp. S32-7.
Imanishi Y, Kobayashi K, Kawata T, et al. Regulatory mechanisms of circulating fibroblast growth factor 23 in parathyroid diseases. Ther Apher Dial. 2007;11 Suppl 1:S32-7.
Imanishi, Y., Kobayashi, K., Kawata, T., Inaba, M., & Nishizawa, Y. (2007). Regulatory mechanisms of circulating fibroblast growth factor 23 in parathyroid diseases. Therapeutic Apheresis and Dialysis : Official Peer-reviewed Journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy, 11 Suppl 1, S32-7.
Imanishi Y, et al. Regulatory Mechanisms of Circulating Fibroblast Growth Factor 23 in Parathyroid Diseases. Ther Apher Dial. 2007;11 Suppl 1:S32-7. PubMed PMID: 17976083.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulatory mechanisms of circulating fibroblast growth factor 23 in parathyroid diseases. AU - Imanishi,Yasuo, AU - Kobayashi,Keisuke, AU - Kawata,Takehisa, AU - Inaba,Masaaki, AU - Nishizawa,Yoshiki, PY - 2007/12/6/pubmed PY - 2008/2/19/medline PY - 2007/12/6/entrez SP - S32 EP - 7 JF - Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy JO - Ther Apher Dial VL - 11 Suppl 1 N2 - Fibroblast growth factor-23 (FGF-23) is a circulating factor regulating phosphate and vitamin D homeostasis. Phosphate intake and an administration of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) increase circulating FGF-23 levels, and elevated FGF-23 prevents hyperphosphatemia and vitamin D toxicity by hyperphosphaturia and suppression of circulating 1,25(OH)(2)D level, comprising a feedback loop to maintain phosphate and vitamin D homeostasis. Excess secretion of parathyroid hormone (PTH), another phosphaturic factor, elevates the serum calcium level in primary hyperparathyroidism. PTH also elevates circulating FGF-23 level, which cooperatively enhances the phosphaturia, resulting in hypophosphatemia. The circulating FGF-23 level increases as renal function declines in chronic kidney disease (CKD), and it exhibits significant and positive correlations with serum phosphate, calcium, and PTH in CKD patients on maintenance hemodialysis, suggesting that these parameters regulate circulating FGF-23 level. Tight associations between circulating FGF-23 and calcium levels were observed both in patients with primary hyperparathyroidism and in CKD patients on maintenance hemodialysis, suggesting the role of serum calcium on FGF-23 regulatory mechanisms. FGF-23 may have a physiological role in preventing tissue damage such as ectopic calcifications, partly via suppressing the serum calcium x phosphate product by accelerating urinary phosphate excretion and suppressing vitamin D activation. SN - 1744-9979 UR - https://www.unboundmedicine.com/medline/citation/17976083/Regulatory_mechanisms_of_circulating_fibroblast_growth_factor_23_in_parathyroid_diseases_ L2 - https://doi.org/10.1111/j.1744-9987.2007.00519.x DB - PRIME DP - Unbound Medicine ER -