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Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy

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Animal models of hyperfunctioning parathyroid diseases for drug development.

Yasuo Imanishi¹, Masaaki Inaba, Takehisa Kawata

¹Osaka City University Graduate School of Medicine, Metabolism, Endocrinology and Molecular Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545 8585, Japan +81 6 6645 3806 ; +81 6 6645 3808 ; imanishi@med.osaka-cu.ac.jp.

Expert Opinion on Drug Discovery

|March 16, 2013

Summary

New transgenic mice models with parathyroid-targeted cyclin D1 overexpression show promise for studying hyperparathyroidism in chronic kidney disease (CKD). These models mimic human disease progression, aiding the development of novel therapeutics for CKD-mineral and bone disorders.

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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
Oncology

Background:

Mineral and bone disorders are linked to high mortality in chronic kidney disease (CKD) patients.
Hyperphosphatemia, vitamin D metabolism disorders, and secondary hyperparathyroidism of uremia (SHPT) are key therapeutic targets in CKD.
Current animal models, like uremic rats, have limitations in lifespan and SHPT severity.

Purpose of the Study:

To review the molecular pathogenesis of hyperfunctioning parathyroid diseases.
To discuss the application of animal models in developing new therapeutics for hyperparathyroidism.

Main Methods:

Utilized PTH-cyclin D1 transgenic mice with parathyroid-targeted overexpression of the cyclin D1 oncogene.
Observed parathyroid cell proliferation, biochemical hyperparathyroidism, and bone abnormalities.
Assessed age-dependent development of hyperparathyroidism and parathyroid cell hyperplasia.

Main Results:

Transgenic mice developed abnormal parathyroid cell proliferation and biochemical hyperparathyroidism with bone abnormalities.
The mice exhibited age-dependent hyperparathyroidism, suitable for precise drug testing.
Parathyroid cell hyperplasia and monoclonal expansion, mirroring refractory SHPT in patients, were observed.

Conclusions:

PTH-cyclin D1 transgenic mice represent a valuable model for studying hyperparathyroidism.
This model aids in the development of new therapeutics for CKD-related bone and mineral disorders.
The model's characteristics closely resemble human refractory SHPT, enhancing its clinical relevance.