Influence of experimental hypothyroidism on bone tissue metabolism and mineral exchange

Aim. Characteristics of the changes of bone remodeling markers and mineral metabolism parameters in experimental mercazolilum-induced hypothyroidism in rats. Methods. Development of hypothyroidism in sexually mature male rats caused by 3-week-long intragastric administration of mercazolilum at a dose of 2.5 ml/100 g of animal weight, was monitored by measurement of the total serum triiodothyronine and thyroxine, and thyroid-stimulating hormone. At the end of intoxication, in the serum of experimental and control rat groups the concentration of Ca, P, Mg, C-terminal telopeptides of collagen type I, bone alkaline phosphatase, parathyroid hormone, testosterone, follicle-stimulating and luteinizing hormones, pro-inflammatory cytokines (interleukin-1β and tumor necrosis factor α) was measured. Results. It was found that mercazolilum-induced hypothyroidism leads to a decrease of serum levels of bone tissue metabolism markers, C-terminal telopeptides (β-Cross Laps), and bone alkaline phosphatase, characterizing slowing of remodeling processes. Decrease of Ca and P concentration in the blood was not observed in such cases. In experimental hypothyroidism caused by mercazolilum administration to male rats, shifts in hormones and cytokine balance occur. Decrease of testosterone, increase of levels of gonadotropins, parathyroid hormone, interleukin-1β, interleukin-6 and tumor necrosis factor α was observed. Conclusion. In experimental hypothyroidism developing after mercazolilum administration, disorder of bone and mineral metabolism not only is a consequence of direct influence of thyroid hormones on bone tissue, but is also mediated by changes in hormone and cytokine status.

experimental hypothyroidism, bone tissue metabolism, phosphate and calcium homeostasis, inflammation