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Cited by 329Parathyroid Disorders and TreatmentsAlkaline Phosphatase Research StudiesRenal function and acid-base balance

The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.

Transgenic Mice Overexpressing Human Fibroblast Growth Factor 23 (R176Q) Delineate a Putative Role for Parathyroid Hormone in Renal Phosphate Wasting Disorders

Bai, Xiuying, Miao, Dengshun, Li, Jiarong, Goltzman, David, Karaplis, Andrew C.·2004·Endocrinology
DOI 10.1210/en.2004-0233
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Abstract

Fibroblast growth factor 23 (FGF23) is a recently characterized protein likely involved in the regulation of serum phosphate homeostasis. Increased circulating levels of FGF23 have been reported in patients with renal phosphate-wasting disorders, but it is unclear whether FGF23 is the direct mediator responsible for the decreased phosphate transport at the proximal renal tubules and the altered vitamin D metabolism associated with these states. To examine this question, we generated transgenic mice expressing and secreting from the liver human FGF23 (R176Q), a mutant form that fails to be degraded by furin proteases. At 1 and 2 months of age, mice carrying the transgene recapitulated the biochemical (decreased urinary phosphate reabsorption, hypophosphatemia, low serum 1,25-dihydroxyvitamin D3) and skeletal (rickets and osteomalacia) alterations associated with these disorders. Unexpectantly, marked changes in parameters of calcium homeostasis were also observed, consistent with secondary hyperparathyroidism. Moreover, in the kidney the anticipated alterations in the expression of hydroxylases associated with vitamin D metabolism were not observed despite the profound hypophosphatemia and increased circulating levels of PTH, both major physiological stimuli for 1,25-dihydroxyvitamin D3 production. Our findings strongly support the novel concept that high circulating levels of FGF23 are associated with profound disturbances in the regulation of phosphate and vitamin D metabolism as well as calcium homeostasis and that elevated PTH levels likely also contribute to the renal phosphate wasting associated with these disorders.

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Metadata

Authors
Bai, X., Miao, D., Li, J., Goltzman, D., & Karaplis, A. C.
Affiliations
  • Jewish General Hospital (CA)
  • McGill University Health Centre (CA)
Corresponding author
Karaplis, Andrew C.
ORCID
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2004-11-01
Volume
145
Issue
11
Pages
5269-5279
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/en.2004-0233
OpenAlex
W2144414222
Cited by
329
References
55
Citations by year
2026: 6 · 2025: 2 · 2024: 3 · 2023: 7 · 2022: 9 · 2021: 7 · 2020: 9 · 2019: 11 · 2018: 17 · 2017: 12 · 2016: 25 · 2015: 11 · 2014: 11 · 2013: 13 · 2012: 33
FWCI
13.11
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • Canadian Institutes of Health Research
  • National Cancer Institute
  • Canadian Arthritis Network
Topics
  • Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Alkaline Phosphatase Research Studies
  • Health Sciences › Medicine › Nephrology › Renal function and acid-base balance
Keywords
fibroblast growth factor 23, parathyroid hormone, renal phosphate wasting, hypophosphatemia, vitamin D metabolism, 1,25-dihydroxyvitamin D3, secondary hyperparathyroidism, calcium homeostasis, osteomalacia, rickets, transgenic mice, furin protease
MeSH terms
Fibroblast Growth Factor-23, Animals, Bone and Bones, Calcium, Female, Fibroblast Growth Factors, Carcinoma, Hepatocellular, Humans, Hypophosphatemia, Familial, Kidney Tubules, Proximal, Male, Mice, Transgenic, Osteomalacia, Parathyroid Hormone, Phosphates, Pregnancy, Vitamin D, Gene Expression, Cell Line, Tumor, Mice

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