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Bone Abstracts (2013) 1 PP105 | DOI: 10.1530/boneabs.1.PP105

1Biomedical Sciences Instite – IBC III – University of Sao Paulo, Sao Paulo, SP, Brazil; 2Physical Education and Sports School – University of Sao Paulo, Sao Paulo, SP, Brazil.


α2C Evidences demonstrate that sympathetic nervous system (SNS) activation causes osteopenia via β2-adrenoceptor (β2-AR) signaling. In a recent study, we showed that female mice with chronic sympathetic hyperactivity due to double knockout of adrenoceptors that negatively regulate norepinephrine release, α2A-AR and α2C-AR (α2A2C-ARKO), present an unexpected phenotype of high bone mass with decreased bone resorption and increased bone formation. Furthermore, we found that these animals are resistant to the thyrotoxicosis-induced osteopenia. These findings suggest that β2-AR is not the single adrenoceptor involved in bone mass regulation and show that α2-AR signaling may also mediate the SNS and thyroid hormone actions in the skeleton. To further investigate the participation of α2-ARs and its possible interaction with thyroid hormone in the regulation of bone mass, we are evaluating the bone phenotype of α2CAR KO mice (α2CAR−/−). A cohort of 30 day-old female congenic α2CAR−/− mice, in a C57BL6/J background, and their wild-type (WT) controls (n=8/group) were treated with a supraphysiological dose of triiodothyronine (T3=7 μg/100 gBW per day) for 30 or 90 days. Surprisingly, a microtomography analysis showed that the trabecular bone volume (BV/TV) of the femur and of the fifth lumbar vertebra (L5) were, respectively, 15–45% lower and 31–83% higher in α2CAR−/− mice, when compared with WT animals (P<0.05 for all). Unlike the double knockout mice (α2A2C-ARKO), α2CAR−/− mice were as sensitive to the thyrotoxicosis-induced osteopenia as WT animals. These findings suggest that α2C-AR may have a role in mediating the deleterious effects of the sympathetic activation in trabecular bone of vertebra and the opposite effects in the femur. In addition, these findings suggest that thyroid hormone does not interact with the SNS, via α2C-AR, to regulate trabecular bone volume.

Volume 1

European Calcified Tissue Society Congress 2013

Lisbon, Portugal
18 May 2013 - 22 May 2013

European Calcified Tissue Society 

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