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The Parathyroid Glands

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Related Experiment Video

Updated: Jun 12, 2026

Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy

Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy

Published on: July 14, 2023

FGF23 and the parathyroid glands.

Justin Silver¹, Tally Naveh-Many

¹Minerva Center for Calcium and Bone Metabolism, Nephrology Services, Hadassah Hebrew University Medical Center, Ein Karem, Jerusalem, 91120, Israel. silver@huji.ac.il

Pediatric Nephrology (Berlin, Germany)

|June 8, 2010

Summary

Fibroblast growth factor 23 (FGF23) is crucial for phosphate balance. In chronic kidney disease (CKD), parathyroid glands become resistant to FGF23, leading to increased parathyroid hormone (PTH) levels.

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Last Updated: Jun 12, 2026

Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy

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Published on: July 14, 2023

Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation

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Establishment of a Simple and Effective Rat Model for Intraoperative Parathyroid Gland Imaging

Establishment of a Simple and Effective Rat Model for Intraoperative Parathyroid Gland Imaging

Published on: August 17, 2022

Area of Science:

Endocrinology
Nephrology
Mineral Metabolism

Background:

Fibroblast growth factor 23 (FGF23) regulates phosphate homeostasis and vitamin D metabolism.
FGF23 exerts its effects via the Klotho-FGFR1c receptor complex.
This complex is present in the kidneys and parathyroid glands, influencing phosphorus reabsorption and parathyroid hormone (PTH) secretion.

Purpose of the Study:

To investigate the role of FGF23 resistance in the parathyroid glands during chronic kidney disease (CKD).
To examine the expression of the Klotho-FGFR1c complex in parathyroid glands in CKD models and patients.

Main Methods:

Review of FGF23 signaling pathways.
Analysis of Klotho-FGFR1c complex expression in experimental CKD and human end-stage renal disease.
Assessment of FGF23's effect on PTH gene expression in advanced CKD.

Main Results:

Both FGF23 and PTH levels are elevated in CKD, suggesting FGF23 resistance.
Expression of the Klotho-FGFR1c complex is reduced in parathyroid glands in experimental CKD and human ESRD.
In advanced CKD, FGF23 demonstrates diminished efficacy in suppressing PTH expression.

Conclusions:

Parathyroid gland resistance to FGF23 is a key feature of CKD pathophysiology.
Reduced Klotho-FGFR1c complex expression contributes to FGF23 resistance in CKD.
This resistance leads to dysregulation of parathyroid hormone secretion and contributes to secondary hyperparathyroidism.