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The Parathyroid Glands

The Parathyroid Glands

The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
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Roles of Electrolytes: Calcium and Phosphate

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Calcium and phosphate are essential electrolytes in the human body, with calcium being the most abundant mineral. Around 99% of the body's calcium is stored in the skeleton and teeth, forming a crystal lattice of mineral salts in combination with phosphates. Calcium plays crucial roles in various bodily functions such as blood clotting, neurotransmitter release, muscle tone maintenance, and nervous and muscle tissue excitability.
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Calcitonin, a vital polypeptide hormone, regulates calcium levels within body fluids. It is released by the parafollicular cells, also known as C cells, situated in the follicular epithelium of the thyroid gland. Calcitonin responds to fluctuations in blood calcium levels and the influence of gastrointestinal hormones like gastrin and cholecystokinin.
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Related Experiment Video

Updated: Jun 26, 2026

Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy

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Phosphate and the parathyroid.

Justin Silver¹, Tally Naveh-Many

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

Kidney International

|January 9, 2009

Summary

This summary is machine-generated.

Phosphate retention in chronic kidney disease causes secondary hyperparathyroidism by affecting parathyroid glands directly. This process involves post-transcriptional regulation of parathyroid hormone mRNA stability.

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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:

Nephrology
Endocrinology
Molecular Biology

Background:

Phosphate (Pi) retention in chronic kidney disease (CKD) is a primary driver of secondary hyperparathyroidism (2HPT).
2HPT involves complex physiological responses including decreased 1,25(OH)2 vitamin D synthesis and hypocalcemia, leading to increased parathyroid hormone (PTH) secretion and parathyroid cell proliferation.
Extracellular calcium (Ca2+) levels, sensed by the parathyroid calcium receptor, directly influence PTH synthesis and secretion.

Purpose of the Study:

To elucidate the intricate mechanisms by which phosphate (Pi) directly regulates parathyroid gland function.
To explore the post-transcriptional regulation of parathyroid hormone (PTH) gene expression in response to altered phosphate levels.
To review the current understanding of phosphate sensing by the parathyroid glands in the context of CKD.

Main Methods:

Review of existing literature on phosphate metabolism, secondary hyperparathyroidism, and parathyroid hormone regulation.
Analysis of the molecular mechanisms involving post-transcriptional control of PTH mRNA.
Discussion of the role of cytosolic proteins and cis-acting elements in regulating PTH mRNA stability.

Main Results:

Phosphate exerts a direct effect on the parathyroid glands, contingent upon intact tissue architecture.
The regulation of PTH gene expression by phosphate, similar to calcium, occurs post-transcriptionally.
Phosphate influences the binding of cytosolic proteins to a specific cis-acting instability sequence in the 3'-untranslated region of PTH mRNA, thereby modulating its half-life.

Conclusions:

Phosphate retention significantly impacts parathyroid function through direct, post-transcriptional mechanisms.
Understanding these regulatory pathways is crucial for managing secondary hyperparathyroidism in chronic kidney disease patients.
The precise mechanisms by which parathyroid glands sense changes in serum phosphate levels remain an area requiring further investigation.