Publication: Decrease in calcitonin and parathyroid hormone mRNA levels and hormone secretion
under long-term hypervitaminosis D3 in rats
Authors
Fernández-Santos, J.M. ; Utrilla, J.C. ; Conde, E. ; Hevia, A. ; Loda, M. ; Martín Lacave, Inés
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
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.
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