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Anatomy, physiology and disease
Published in C M Langton, C F Njeh, The Physical Measurement of Bone, 2016
Parathyroid hormone (PTH) is a peptide that stimulates bone through its ability to activate the PTH/PTHrp (parathyroid-hormone-related protein) receptor located on the surface of osteoblasts [119]. PTH plays a direct and important role in bone remodelling. Bone histomorphometric studies have demonstrated that the administration of PTH in vivo stimulates bone formation [120, 121]. However, the effects on bone formation are complex. It can stimulate and inhibit bone collagen and matrix synthesis [122]. PTH stimulates differentiation of committed progenitors to fuse, forming mature multinucleated osteoclasts. However, PTH does not directly stimulate bone resorption because the osteoclast does not respond to PTH [109]. It is probably mediated through cells in the osteoblast lineage such as the lining cells [123].
Calcium, phosphate and magnesium
Published in Martin Andrew Crook, Clinical Biochemistry & Metabolic Medicine, 2013
Parathyroid hormone-related protein (PTHRP) is a peptide hormone that has a similar amino acid sequence at the biologically active end of the peptide, therefore activating the same receptors as PTH. The function of PTHRP is uncertain, but it may be important in calcium metabolism in the fetus. The gene that codes for PTHRP is widely distributed in body tissues but is normally repressed. However, it may become derepressed in certain tumours, causing humoral hypercalcaemia of malignancy.
Progress in the study of nutritional status and selenium in dialysis patients
Published in Annals of Medicine, 2023
Meiran Cao, Shuai Zheng, Wenhua Zhang, Guicai Hu
Hyperparathyroidism is common in end-stage dialysis patients. It has been found that parathyroid hormone plays a key role in the browning of adipose tissue and increased resting energy expenditure in dialysis patients. Cuppari et al. [75] measured resting energy expenditure in dialysis patients with hyperparathyroidism and found that parathyroid hormone was an independent determinant of resting energy expenditure. And the researcher also found that 6 months after surgery in patients with severe hyperparathyroidism, parathyroid hormone levels and the patients’ resting energy expenditure were significantly reduced. Regarding the mechanism by which parathyroid hormone increases resting energy expenditure and adipose tissue browning, Kir et al. [76] found that parathyroid hormone and parathyroid hormone-related protein (PTHrP) in dialysis patients can increase the expression of thermogenic genes, accelerate adipose tissue browning, and increase resting energy expenditure in dialysis patients. In 2022, a retrospective study by Disthabanchong et al. [77] showed that patients with severe hyperparathyroidism had a poorer nutritional status than dialysis patients with normal or moderate hyperparathyroidism.
A Meta-Analysis of Calcium Intake and Risk of Glioma
Published in Nutrition and Cancer, 2022
There are many explanations for the mechanism by which calcium reduces the risk of glioma. This may be related to the involvement of calcium in cell apoptosis. Juin et al. discovered that glutamate-induced apoptosis in cerebellar granule neurons is characterized by intracellular calcium increase (33). Intracellular calcium may affect DNA repair through calmodulin (34). Besides, higher levels of calcium will lead to down-regulation of parathyroid hormone production (35). Parathyroid hormone has been considered as a tumor promoter and can act as a mitogen and anti-apoptotic factor. De Miguel et al. detected parathyroid hormone-related protein in human astrocytomas and proposed that the parathyroid hormonerelated protein, via the parathyroid hormone receptor, is associated with astrocytoma cell proliferation and dedifferentiation (36). Our results support the evidence that calcium intake is negatively correlated with the risk of brain tumors, but the relationship between calcium intake and astrocytoma risk and serum parathyroid hormone levels needs further research to explore.
Abaloparatide: an anabolic treatment to reduce fracture risk in postmenopausal women with osteoporosis
Published in Current Medical Research and Opinion, 2020
Paul D. Miller, John P. Bilezikian, Lorraine A. Fitzpatrick, Bruce Mitlak, Eugene V. McCloskey, Felicia Cosman, Henry G. Bone
Parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP) both signal through the PTH receptor type 1 (PTHR1) with important, but different, effects on bone development and remodeling21–23. Studies have demonstrated that PTH and PTHrP bind to different conformations of the PTHR1 receptor with differing affinities22. PTH binds with greater affinity than PTHrP22 to the G-protein uncoupled conformation, R0, which is associated with prolonged cyclic AMP signaling, while PTHrP and PTH bind with similar affinities to the G protein-coupled RG conformation, which results in shorter duration of cyclic AMP response22. Therefore, only PTH results in sustained cyclic AMP production, which involves receptor internalization and positive calcium allostery23–26. Studies have shown that continuous cyclic AMP signaling favors osteoclast formation and bone resorption while intermittent signaling favors a net anabolic effect21,27–29; however, whether this translates to clinically relevant difference with PTH and PTHrP ligands on bone resorption remains to be determined.