Class B/2; Endochondral Ossification; G alpha (s) signalling events; GPCR downstream signaling; GPCR ligand binding; Osteoblast Signaling; Signaling by GPCR
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Background
The parathyroid gland is an important endocrine gland in the human body. It is located behind the left and right lobes of the thyroid gland. It is brown-yellow and about the size of a soya bean. There are usually two pairs of parathyroid glands. The upper pair is usually located in the middle and upper 1/3 of the back of the lateral lobe of the thyroid, and the lower pair is usually located at the lower end of the back of the lateral lobe. Occasionally, ectopic parathyroid glands are found buried within the thyroid gland. The surface of the parathyroid gland is covered by a thin layer of connective tissue called a capsule. The connective tissue of the capsule carries blood vessels, lymphatic vessels and nerves into the gland, forming trabeculae that divide the gland into incomplete lobules. The glandular parenchyma cells in the lobules are arranged in cords or clusters, with a small amount of connective tissue and abundant capillaries in between. Under the light microscope, glandular cells can be divided into two types: chief cells and eosinophilic cells. Chief cells: round or polygonal, with round nuclei in the centre of the cell, and the cytoplasm is lightly stained in HE-stained sections. On electron microscopy, the cytoplasm contains rough endoplasmic reticulum, anion gap secondary complexes and secretory granules 200-400 nm in diameter, and some glycogen and lipid droplets. Parathyroid hormone (PTH) in the secretory granules is released into the capillaries by exocytosis.
Figure1. Physiological actions of parathyroid hormone (PTH). (Sources: Duque EJ, et al. 2020)
Parathormone is a peptide hormone. Its main function is to act on osteocytes and osteoclasts to dissolve bone salts and promote calcium absorption in the intestine and renal tubules, thereby increasing blood calcium. Under the joint regulation of parathyroid hormone and calcitonin, blood calcium is kept stable. Eosinophils: Starting around puberty, eosinophils appear in the parathyroid glands of some animals and humans and increase with age. The cells often exist alone or in groups between the main cells. Eosinophils are larger than the main cells, with smaller nuclei and darker staining. The cytoplasm contains dense eosinophilic granules and is therefore highly eosinophilic. The main ultrastructural feature is that there are a large number of dense, long mitochondria with many cristae. There are many glycogen granules between the mitochondria. The Golgi complex is small and the endoplasmic reticulum is sparse. There are very few secretory granules. The strong eosinophilia of the cytoplasm is caused by the dense mitochondria. The significance of this cell type is unknown. Recent studies tend to show that the parathyroid glands have only chief cells, while other cell types may be manifestations of different functional states or degenerative changes.
PTH can be measured by a two-site enzyme-linked immunosorbent assay (sandwich method). The sample, anti-human PTH monoclonal antibody-ALP conjugate, protein-containing tris buffer and anti-human PTH polyclonal antibody-coated magnetic microspheres are added to the reaction vessel. After incubation in the reaction tube, substances bound to the solid phase are attracted by the magnetic field, while unbound substances are washed away. The chemiluminescent substrate is then added to the reaction tube, which rapidly emits light under the action of ALP. The amount of light produced is proportional to the concentration of PTH in the sample. The amount of PTH in the sample is determined from a multi-point calibration curve.
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References
Parathyroid hormone (PTH) regulation of metabolic homeostasis: An old dog teaches us new tricks
Background: Late in the nineteenth century, it was theorized that a circulating product produced by the parathyroid glands could negatively impact skeletal homeostasis. A century later, intermittent administration of that protein, namely parathyroid hormone (PTH), was approved by the FDA and EMA as the first anabolic agent to treat osteoporosis. Yet, several unanswered but important questions remain about the skeletal actions of PTH. Scope of review: Current research efforts have focused on improving the efficacy of PTH treatment by designing structural analogs and identifying other targets (e.g., the PTH or the calcium sensing receptor). A unique but only recently described aspect of PTH action is its regulation of cellular bioenergetics and metabolism, namely in bone and adipose tissue but also in other tissues. The current review aims to provide a brief background on PTH's previously described actions on bone and highlights how PTH regulates osteoblast bioenergetics, contributing to greater bone formation. It will also shed light on how PTH could alter metabolic homeostasis through its actions in other cells and tissues, thereby impacting the skeleton in a cell non-autonomous manner. Major conclusions: PTH administration enhances bone formation by targeting the osteoblast through transcriptional changes in several pathways; the most prominent is via adenyl cyclase and PKA. PTH and its related protein, PTHrP, also induce glycolysis and fatty acid oxidation in bone cells and drive lipolysis and thermogenic programming in adipocytes; the latter may indirectly but positively influence skeletal metabolism. While much work remains, alterations in cellular metabolism may also provide a novel mechanism related to PTH's temporal actions. Thus, the bioenergetic impact of PTH can be considered another of the myriad anabolic effects of PTH on the skeleton. Just as importantly from a translational perspective, the non-skeletal metabolic effects may lead to a better understanding of whole-body homeostasis along with new and improved therapies to treat musculoskeletal conditions.
Parathyroid hormone and parathyroid hormone-related protein analogs as therapies for osteoporosis
Osteoporotic fractures result in significant morbidity and mortality. Anabolic agents reverse the negative skeletal balance that characterizes osteoporosis by stimulating osteoblast-dependent bone formation to a greater degree than osteoclast-dependent bone resorption. Parathyroid hormone (PTH) and parathyroid hormone- related protein (PTHrP) are peptide hormones, which have anabolic actions when administered intermittently. The only FDA-approved anabolic bone agent for the treatment of osteoporosis in the United States is PTH 1-34, or teriparatide, administered by daily subcutaneous injections. However, PTH 1-84 is also available in Europe. Synthetic human PTHrP 1-36 and a PTHrP 1-34 analog, BA058, have also been shown to increase lumbar spine bone density. These agents and several other PTH and PTHrP analogs, including some which are not administered as injections, continue to be investigated as potential anabolic therapies for osteoporosis.
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Figure1. Physiological actions of parathyroid hormone (PTH). (Sources: Duque EJ, et al. 2020)
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