TY  - JOUR
AU  - Filipović, Branko
AU  - Šošić-Jurjević, Branka 
AU  - Ajdžanović, Vladimir
AU  - Živanović, Jasmina
AU  - Isenović, Esma
AU  - Popovska-Perčinić, Florina
AU  - Milošević, Verica
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1963
AB  - Thyroid C-cells produce calcitonin (CT), a hypocalcemic hormone, that
   acts as an inhibitor of bone resorption. In this study, we investigated
   the effects of tamoxifen (TAM) as a selective estrogen receptor
   modulator on thyroid C-cells, trabecular bone and biochemical markers of
   bone metabolism in an animal model of androgen deficiency, represented
   by middle-aged orchidectomized (Orx) rats. Fifteen-month-old male Wistar
   rats were divided into: Orx and sham-operated (SO) groups. Rats from one
   Orx group were injected subcutaneously with TAM citrate (Orx + TAM; 0.3
   mgkg(-1) b.w.), while the rats from SO and a second Orx group received
   vehicle alone, once a day for 3 weeks. The peroxidase-antiperoxidase
   method was applied for localization of CT in C-cells. Thyroid C-cells
   were morphometrically and ultrastructurally analyzed. An ImageJ
   image-processing program was used to measure bone histomorphometric
   parameters. Blood serum samples were analyzed for CT, osteocalcin (OC),
   calcium (Ca2+) and phosphorus (P). Urinary Ca2+ concentrations were
   measured. TAM treatment significantly increased thyroid C-cell volume
   (V-c) and serum CT when compared with vehicle-treated Orx rats. Analysis
   of trabecular microarchitecture of the tibia showed that administration
   of TAM significantly increased cancellous bone area, trabecular
   thickness and trabecular number, whereas trabecular separation was
   significantly decreased compared with vehicle-treated Orx rats. Serum OC
   and urinary Ca2+ concentrations were significantly lower in comparison
   with the control Orx group. These results indicate that in our rat model
   of androgen deficiency, TAM stimulated calcitonin-producing thyroid
   C-cells and increased trabecular bone mass.
PB  - John Wiley and Sons
T2  - Journal of Anatomy
T1  - Tamoxifen stimulates calcitonin-producing thyroid C-cells and prevents
 trabecular bone loss in a rat model of androgen deficiency
IS  - 5
VL  - 226
DO  - 10.1111/joa.12298
SP  - 489
EP  - 496
ER  - 

@article{
author = "Filipović, Branko and Šošić-Jurjević, Branka  and Ajdžanović, Vladimir and Živanović, Jasmina and Isenović, Esma and Popovska-Perčinić, Florina and Milošević, Verica",
year = "2015",
abstract = "Thyroid C-cells produce calcitonin (CT), a hypocalcemic hormone, that
   acts as an inhibitor of bone resorption. In this study, we investigated
   the effects of tamoxifen (TAM) as a selective estrogen receptor
   modulator on thyroid C-cells, trabecular bone and biochemical markers of
   bone metabolism in an animal model of androgen deficiency, represented
   by middle-aged orchidectomized (Orx) rats. Fifteen-month-old male Wistar
   rats were divided into: Orx and sham-operated (SO) groups. Rats from one
   Orx group were injected subcutaneously with TAM citrate (Orx + TAM; 0.3
   mgkg(-1) b.w.), while the rats from SO and a second Orx group received
   vehicle alone, once a day for 3 weeks. The peroxidase-antiperoxidase
   method was applied for localization of CT in C-cells. Thyroid C-cells
   were morphometrically and ultrastructurally analyzed. An ImageJ
   image-processing program was used to measure bone histomorphometric
   parameters. Blood serum samples were analyzed for CT, osteocalcin (OC),
   calcium (Ca2+) and phosphorus (P). Urinary Ca2+ concentrations were
   measured. TAM treatment significantly increased thyroid C-cell volume
   (V-c) and serum CT when compared with vehicle-treated Orx rats. Analysis
   of trabecular microarchitecture of the tibia showed that administration
   of TAM significantly increased cancellous bone area, trabecular
   thickness and trabecular number, whereas trabecular separation was
   significantly decreased compared with vehicle-treated Orx rats. Serum OC
   and urinary Ca2+ concentrations were significantly lower in comparison
   with the control Orx group. These results indicate that in our rat model
   of androgen deficiency, TAM stimulated calcitonin-producing thyroid
   C-cells and increased trabecular bone mass.",
publisher = "John Wiley and Sons",
journal = "Journal of Anatomy",
title = "Tamoxifen stimulates calcitonin-producing thyroid C-cells and prevents
 trabecular bone loss in a rat model of androgen deficiency",
number = "5",
volume = "226",
doi = "10.1111/joa.12298",
pages = "489-496"
}

Filipović, B., Šošić-Jurjević, B., Ajdžanović, V., Živanović, J., Isenović, E., Popovska-Perčinić, F.,& Milošević, V.. (2015). Tamoxifen stimulates calcitonin-producing thyroid C-cells and prevents
 trabecular bone loss in a rat model of androgen deficiency. in Journal of Anatomy
John Wiley and Sons., 226(5), 489-496.
https://doi.org/10.1111/joa.12298

Filipović B, Šošić-Jurjević B, Ajdžanović V, Živanović J, Isenović E, Popovska-Perčinić F, Milošević V. Tamoxifen stimulates calcitonin-producing thyroid C-cells and prevents
 trabecular bone loss in a rat model of androgen deficiency. in Journal of Anatomy. 2015;226(5):489-496.
doi:10.1111/joa.12298 .

Filipović, Branko, Šošić-Jurjević, Branka , Ajdžanović, Vladimir, Živanović, Jasmina, Isenović, Esma, Popovska-Perčinić, Florina, Milošević, Verica, "Tamoxifen stimulates calcitonin-producing thyroid C-cells and prevents
 trabecular bone loss in a rat model of androgen deficiency" in Journal of Anatomy, 226, no. 5 (2015):489-496,
https://doi.org/10.1111/joa.12298 . .