Parathyroid Hormone: Its Role in Calcium and Phosphate Homeostasis

2019 ◽  
Vol 74 (2) ◽  
pp. 136-144 ◽  
Author(s):  
Natalia G. Mokrysheva ◽  
Julia A. Krupinova ◽  
Elena V. Kovaleva

Wide prevalence of the parathyroid glands pathology and the need for new methods of diagnosis and treatment are forcing researchers all over the world to go more deeply into the pathophysiological mechanisms. A parathyroid hormone (PTH) is main cause of mineral disorders. In addition, humans have a family with similar in structure molecules that contribute to the maintenance of calcium and phosphate homeostasis. The family includes PTH, parathyroid hormone-related protein (PTHrP) and tuberoinfundibular peptide 39 (TIP39, also known as PTH2). The genes encoding these peptides have highly homologous amino acid regions in the N-(amino) terminal receptor-binding sites of each family member, as well as the preserved structure of their organization, which seems to be due to the presence of one parent gene. The variety of classical and “non-classical” effects allows to expand the understanding of these substances and consider them as hormones that go beyond the regulation of phosphorus-calcium metabolism. The review provides information on the structure and biosynthesis of these peptides, as well as a wide range of their effects on the human body.


2020 ◽  
Vol 21 (15) ◽  
pp. 5388 ◽  
Author(s):  
Giovanni Lombardi ◽  
Ewa Ziemann ◽  
Giuseppe Banfi ◽  
Sabrina Corbetta

Exercise perturbs homeostasis, alters the levels of circulating mediators and hormones, and increases the demand by skeletal muscles and other vital organs for energy substrates. Exercise also affects bone and mineral metabolism, particularly calcium and phosphate, both of which are essential for muscle contraction, neuromuscular signaling, biosynthesis of adenosine triphosphate (ATP), and other energy substrates. Parathyroid hormone (PTH) is involved in the regulation of calcium and phosphate homeostasis. Understanding the effects of exercise on PTH secretion is fundamental for appreciating how the body adapts to exercise. Altered PTH metabolism underlies hyperparathyroidism and hypoparathyroidism, the complications of which affect the organs involved in calcium and phosphorous metabolism (bone and kidney) and other body systems as well. Exercise affects PTH expression and secretion by altering the circulating levels of calcium and phosphate. In turn, PTH responds directly to exercise and exercise-induced myokines. Here, we review the main concepts of the regulation of PTH expression and secretion under physiological conditions, in acute and chronic exercise, and in relation to PTH-related disorders.


Endocrine ◽  
2016 ◽  
Vol 55 (1) ◽  
pp. 273-282 ◽  
Author(s):  
Bart L. Clarke ◽  
Tamara J. Vokes ◽  
John P. Bilezikian ◽  
Dolores M. Shoback ◽  
Hjalmar Lagast ◽  
...  

Metabolism ◽  
1975 ◽  
Vol 24 (2) ◽  
pp. 199-204 ◽  
Author(s):  
Robert S. Swenson ◽  
JoséR. Weisinger ◽  
James L. Ruggeri ◽  
Gerald M. Reaven

2017 ◽  
Vol 58 (4) ◽  
pp. R203-R224 ◽  
Author(s):  
Murat Bastepe ◽  
Serap Turan ◽  
Qing He

Parathyroid hormone (PTH) is a key regulator of skeletal physiology and calcium and phosphate homeostasis. It acts on bone and kidney to stimulate bone turnover, increase the circulating levels of 1,25 dihydroxyvitamin D and calcium and inhibit the reabsorption of phosphate from the glomerular filtrate. Dysregulated PTH actions contribute to or are the cause of several endocrine disorders. This calciotropic hormone exerts its actions via binding to the PTH/PTH-related peptide receptor (PTH1R), which couples to multiple heterotrimeric G proteins, including Gs and Gq/11. Genetic mutations affecting the activity or expression of the alpha-subunit of Gs, encoded by the GNAS complex locus, are responsible for several human diseases for which the clinical findings result, at least partly, from aberrant PTH signaling. Here, we review the bone and renal actions of PTH with respect to the different signaling pathways downstream of these G proteins, as well as the disorders caused by GNAS mutations.


2021 ◽  
Vol 23 (1) ◽  
pp. 44
Author(s):  
Mirjana Babić Leko ◽  
Nikolina Pleić ◽  
Ivana Gunjača ◽  
Tatijana Zemunik

Calciotropic hormones, parathyroid hormone (PTH) and calcitonin are involved in the regulation of bone mineral metabolism and maintenance of calcium and phosphate homeostasis in the body. Therefore, an understanding of environmental and genetic factors influencing PTH and calcitonin levels is crucial. Genetic factors are estimated to account for 60% of variations in PTH levels, while the genetic background of interindividual calcitonin variations has not yet been studied. In this review, we analyzed the literature discussing the influence of environmental factors (lifestyle factors and pollutants) on PTH and calcitonin levels. Among lifestyle factors, smoking, body mass index (BMI), diet, alcohol, and exercise were analyzed; among pollutants, heavy metals and chemicals were analyzed. Lifestyle factors that showed the clearest association with PTH levels were smoking, BMI, exercise, and micronutrients taken from the diet (vitamin D and calcium). Smoking, vitamin D, and calcium intake led to a decrease in PTH levels, while higher BMI and exercise led to an increase in PTH levels. In terms of pollutants, exposure to cadmium led to a decrease in PTH levels, while exposure to lead increased PTH levels. Several studies have investigated the effect of chemicals on PTH levels in humans. Compared to PTH studies, a smaller number of studies analyzed the influence of environmental factors on calcitonin levels, which gives great variability in results. Only a few studies have analyzed the influence of pollutants on calcitonin levels in humans. The lifestyle factor with the clearest relationship with calcitonin was smoking (smokers had increased calcitonin levels). Given the importance of PTH and calcitonin in maintaining calcium and phosphate homeostasis and bone mineral metabolism, additional studies on the influence of environmental factors that could affect PTH and calcitonin levels are crucial.


1964 ◽  
Vol 46 (2) ◽  
pp. 285-291 ◽  
Author(s):  
Allan Halden ◽  
E. Eisenberg ◽  
Gilbert S. Gordan

ABSTRACT To determine whether parathyroid hormone is required for renal response to phosphorus loading, the effects of ingestion of 3100 mg of phosphorus daily for 3 days were compared in 5 treated hypoparathyroid patients and 5 normal control subjects of comparable age and sex. In both normal and hypoparathyroid subjects the response to phosphorus loading was characterized by an increase in urinary excretion of phosphorus without a concomitant increase in the rate of glomerular filtration of phosphorus. Some mechanism other than changes in rates of parathyroid hormone secretion probably accounts for renal responses to changes in phosphorus intake. The timing of urine and serum collections with regard to food intake and the total amount of phosphorus in the diet were found to affect the assessment of renal handling of phosphorus. The finding that a 3-day period of oral phosphorus loading did not increase the serum phosphorus level in the hypoparathyroid patients suggests that phosphorus restriction is not always necessary in the treatment of hypoparathyroidism. The addition of one more condition to the list of those that may affect the percentage of renal tubular resorption of phosphorus in no way decreases the usefulness of this determination in the diagnosis of hyperparathyroidism.


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