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Título: | Decrease in calcitonin and parathyroid hormone mRNA levels and hormone secretion under long-term hypervitaminosis D3 in rats |
Fecha de publicación: | 2001 |
Editorial: | Murcia : F. Hernández |
ISSN: | 0213-3911 |
Materias relacionadas: | CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología |
Palabras clave: | Vitamin D3 Calcitonin |
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 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. |
Autor/es principal/es: | Fernández-Santos, J.M. Utrilla, J.C. Conde, E. Hevia, A. Loda, M. Martín Lacave, Inés |
Forma parte de: | Histology and histopathology |
URI: | http://hdl.handle.net/10201/20668 |
Tipo de documento: | info:eu-repo/semantics/article |
Número páginas / Extensión: | 8 |
Derechos: | info:eu-repo/semantics/openAccess |
Aparece en las colecciones: | Vol.16, nº 2 (2001) |
Ficheros en este ítem:
Fichero | Descripción | Tamaño | Formato | |
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Decrease in calcitonin and parathyroid.pdf | 5,07 MB | Adobe PDF | Visualizar/Abrir |
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