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Decrease in calcitonin and parathyroid hormone mRNA levels and hormone secretion under long-term hypervitaminosis D3 in rats

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dc.contributor.authorFernández-Santos, J.M.es
dc.contributor.authorUtrilla, J.C.es
dc.contributor.authorConde, E.
dc.contributor.authorHevia, A.
dc.contributor.authorLoda, M.
dc.contributor.authorMartín Lacave, Inés
dc.date.accessioned2011-05-11T10:56:08Z
dc.date.available2011-05-11T10:56:08Z
dc.date.issued2001
dc.description.abstractIn 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.es
dc.formatapplication/pdfes
dc.format.extent8es
dc.identifier.issn0213-3911es
dc.identifier.urihttp://hdl.handle.net/10201/20668
dc.languageenges
dc.publisherMurcia : F. Hernándezes
dc.relation.ispartofHistology and histopathologyes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectVitamin D3es
dc.subjectCalcitonines
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleDecrease in calcitonin and parathyroid hormone mRNA levels and hormone secretion under long-term hypervitaminosis D3 in ratses
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.16, nº 2 (2001)