Artículo
Decrease in calcitonin and parathyroid hormone mRNA levels and hormone secretion under long-term hypervitaminosis D3 in rats
Autor/es | Fernández-Santos, José María
Utrilla Alcolea, José Carmelo Conde Amiano, Esperanza Hevia Alonso, Antonio Loda, M. Martín Lacave, Inés María |
Departamento | Universidad de Sevilla. Departamento de Citología e Histología Normal y Patológica |
Fecha de publicación | 2001-04-25 |
Fecha de depósito | 2017-05-16 |
Publicado en |
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Resumen | In calcium homeostasis, vitamin D3 is a potent serum calcium-raising agent which in vivo regulates both calcitonin (CT) and parathyroid hormone (PTH) gene expression. Serum calcium is the major secretagogue for CT, a hormons ... In calcium homeostasis, vitamin D3 is a potent serum calcium-raising agent which in vivo regulates both calcitonin (CT) and parathyroid hormone (PTH) gene expression. Serum calcium is the major secretagogue for CT, a hormons product whose biosynthesis is the main biological activity of thyroid Ccells. Taking advantage of this regulatory mechanism, long-term vitamin D3-induced hypercalcemia has been extensively used as a model to produce hyperactivation, hyperplasia and even proliferative lesions of C-cells, supposedly to reduce the sustained high calcium serum concentrations. We have recently demonstrated that CT serum levels did not rise after long-term hypervitaminosis D3. Moreover, C-cells did not have a proliferative response, rather a decrease in CT-producing C-cell number was observed. In order to confirm the inhibitory effect of vitamin D3 on C-cells, Wistar rats were administered vitamin D3 chronically (25,000 IUId) with or without calcium chloride (CaC12). Under these long-term vitaminD -hypercalcemic conditions, calcium, active metaboetes of vitamin 4 , CT and PTH serum concentrations were determined by RIA; CT and PTH mRNA levels were analysed by Northern blot and in situ hybridization; and, finally, the ultrastructure of calciotrophic hormone-producing cells was analysed by electron microscapy. Our results show, that, in rats, long term administration of vitamin D3 results in a decrease in hormone biosynthetic activities of both PTH and CTproducing cells, albeit at different magnitudes. Based upon these results, we conclude that hypervitaminosis D3-based methods do not stimulate C-cell activity and can not be used to induce proliferative lesions of calcitonin-producing cells. |
Cita | Fernández-Santos, J.M., Utrilla Alcolea, J.C., Conde Amiano, E., Hevia Alonso, A., Loda, M. y Martín Lacave, I.M. (2001). Decrease in calcitonin and parathyroid hormone mRNA levels and hormone secretion under long-term hypervitaminosis D3 in rats. Histology and Histopathology, 16 (2), 407-414. |
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