Influence of experimental hypothyroidism on bone tissue metabolism and mineral exchange

Cover Page


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.

F Kh Kamilov
Bashkir State Medical University Ufa, Russia

V N Kozlov
Bashkir State Medical University Ufa, Russia

T I Ganiev
Bashkir State Medical University Ufa, Russia

R R Yunusov
Bashkir State Medical University Ufa, Russia

  • Nicholls J.J., Brassill N.J., Williams G.R., Bassert J.H. The skeletal consequences of thyrotoxicosis. J. Endocrinol. 2012; 213: 209-211. doi: 10.1530/JOE-12-0059.
  • Freitas F.R., Moristoc A.S., Jorgetti V. et al. Spared bone mass in ratstreated with thyroid hormone receptor TRβ - selective compound GC-1. Am. J. Physiol. Endocrinol. 2003; 285: E1135-1145. doi: 10.1152/ajpendo.00506.2002.
  • Ночевная Л.Б., Павленко О.А., Калинина О.Ю., Столяров В.А. Состояние костной ткани у больных с впервые выявленным гипотиреозом. Сибирский мед. ж. 2011; 26 (4): 189-193.
  • Bassett J.H., Boyde A., Howell P.G. et al. Optimal bone strength anel mineralization requites the type 2 iodothyronine deiodisale in osteoblast. Proc. Natl. Acad. Sci. USA. 2010; 107 (6): 7604-7609.
  • Gouveia C.H., Jorgetti V., Bianco A.C. Effect ot thyroid hormone administion and estrogen deficiency on bone mass of female rats. J. Bone Miner. Res. 1997; 12: 2098-2107. doi: 10.1359/jbmr.1997.12.12.2098.
  • Krassas G.E., Poppe K., Glinoer D. Thyroid function and human reproductive health. Endocrine Reveiws. 2010; 31 (6): 702-735. doi: 10.1210/er.2009-0041.
  • Varga F., Rumpler M., Kiaushofer K. Thyroid hormone increase insulin-like growth factor mRNA levels in the clonal osteoblastic all line MC3T3 - E1. FEBS Lett. 1994; 345: 67-70. doi: 10.1016/0014-5793(94)00442-0.
  • Козлов В.Н. Тиреоидная трансформация при моделировании эндемического эффекта у белых крыс в эксперименте. Сибирский мед. ж. 2006; (5): 27-30.
  • Cardoso L.F., Maciel L.M., de Paula F.J.A. The nucltiple effects of thyroid disorders on bone and mineral metabolism. Arg. Bras. Endocrinol. Metab. 2014; 58 (5): 452-462. doi: 10.1590/0004-2730000003311.
  • Schwarz A.N., Sellmeyer D.E., Strotmeyer E.S. et al. Diabetes and bone loss at the hip in older black and white adults. J. Bone Miner. Res. 2005; 20 (4): 596-603. doi: 10.1359/JBMR.041219.
  • Казимирко В.К., Коваленко В.Н., Мальцев В.Н. Остеопороз: патогенез, клиника, профилактика и лечение. 2-е изд. Киев: Морион. 2006; 159 с.
  • Pantazi H., Papapetrou P.D. Changes in parameters of bone and mineral metabolism during therapy for hyperthyroidism. J. Clin. Endocrinol. Metab. 2000; 85 (3): 1099-1106. doi: 10.1210/jcem.85.3.6457.
  • Gruber R., Cherwenka K., Wolf F. et al. Expression of vitamin D receptor, of estrogen and thyroid hormone receptor alpha- and beta-isoform, and androgen receptor in cultures of native mouse bone marrow and of stromal/osteoblastic cella. Bone. 1999; 24: 465-473. doi: 10.1016/S8756-3282(99)00017-4.
  • Bassett J.H., Williams G.R. The skeletal phenotypes of TR alpha and TR beta mutant mice. J. Mol. Endocrinol. 2009; 42: 269-282. doi: 10.1677/JME-08-0142.
  • Wei S., Kitaura H., Zhou P. et al. IL-1 mediates TNF-induced osteoclastogenesis. J. Clin. Invest. 2005; 115: 282-290. doi: 10.1172/JCI200523394.
  • Zhdo B., Gimes S., Li S. et al. TNF - induced osteoclastogenesis and inflammatory bone resorption are inhibited by transcription factor RBP-J. J. Exp. Med. 2012; 209 (2): 319-334. doi: 10.1084/jem.20111566.


Abstract - 22

PDF (Russian) - 8

© 2017 Kamilov F.K., Kozlov V.N., Ganiev T.I., Yunusov R.R.

Creative Commons License

This work is licensed
under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.