PTH and Vitamin D

Abstract

PTH and Vitamin D are two major regulators of mineral metabolism. They play critical roles in the maintenance of calcium and phosphate homeostasis as well as the development and maintenance of bone health. PTH and Vitamin D form a tightly controlled feedback cycle, PTH being a major stimulator of vitamin D synthesis in the kidney while vitamin D exerts negative feedback on PTH secretion. The major function of PTH and major physiologic regulator is circulating ionized calcium. The effects of PTH on gut, kidney, and bone serve to maintain serum calcium within a tight range. PTH has a reciprocal effect on phosphate metabolism. In contrast, vitamin D has a stimulatory effect on both calcium and phosphate homeostasis, playing a key role in providing adequate mineral for normal bone formation. Both hormones act in concert with the more recently discovered FGF23 and klotho, hormones involved predominantly in phosphate metabolism, which also participate in this closely knit feedback circuit. Of great interest are recent studies demonstrating effects of both PTH and vitamin D on the cardiovascular system. Hyperparathyroidism and vitamin D deficiency have been implicated in a variety of cardiovascular disorders including hypertension, atherosclerosis, vascular calcification, and kidney failure. Both hormones have direct effects on the endothelium, heart, and other vascular structures. How these effects of PTH and vitamin D interface with the regulation of bone formation are the subject of intense investigation.

Activation of the calcium-sensing receptor attenuates TRPV6-dependent intestinal calcium absorption

“…The TRPV6 D541A/D541A mice were backcrossed to FVB/N for more than 5 generations. Standard pelleted chow (PicoLab Rodent Diet 5053: 21% wt/wt protein, 5.0% wt/wt fat, 0.81% wt/wt Ca 2+ , and 2.2 IU/g vitamin D 3 ) and drinking water were available ad libitum. The experiments with respect to chronic altered Ca 2+ -containing diets (21 days) and treatment with 1,25-[OH] 2 D 3 (5 days) and cinacalcet (Santa Cruz Biotechnology) (5 days) were performed and described previously (15).…”

“…Calcium (Ca 2+ ) homeostasis is vital to many physiological functions and is thus tightly regulated by altering Ca 2+ transport across intestine, kidneys, and bone. It has been appreciated for some time that endocrine hormones, including parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D 3 (1,25-[OH] 2 D 3 ), alter Ca 2+ transport across the intestine and kidneys or aid mobilization from bone (1)(2)(3)(4). However, more recently, the homeostatic mechanisms permitting direct sensing of extracellular Ca 2+ by the nephron or bone and subsequently altering tubular Ca 2+ reabsorption or bone remodeling were delineated (5,6).…”

Protective Role of Vitamin D in Renal Tubulopathies

“…At the same time, 1,25(OH)2D3 regulates plasma parathyroid hormone (PTH) levels that, in turn, contribute to modulate Calcium and Phosphate metabolism [8]. 1,25(OH)2D3 exerts negative feedback on PTH decreasing its production and release, while, au contraire, PTH secretion increases 1,25(OH)2D3 production [9,10].…”

Osteomalacia in practice of endocrinologist: etiology, pathogenesis, differential diagnosis with osteoporosis

“…В свою очередь, ВГПТ приводит к усиленной мобилизации кальция из костей, повышенной реабсорбции кальция в почках и увеличению гидроксилирования 25(OH)D в 1,25(OH) 2 D 3 1α-гидроксилазой (CYP27B1). Выраженный дефицит витамина D (<10 нг/мл), как правило, сопровождается низким уровнем 1,25(OH) 2 D 3 , тогда как на фоне умеренного дефицита витамина D (<20 нг/мл) стимуляция CYP27B1 под действием ПТГ может приводить к нормальному или даже повышенному уровню 1,25(OH) 2 D 3 [8].…”