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• W2114636153 abstract "To investigate whether thyroid hormone (TH) interacts with the sympathetic nervous system (SNS) to modulate bone mass and structure, we studied the effects of daily T 3 treatment in a supraphysiological dose for 12 wk on the bone of young adult mice with chronic sympathetic hyperactivity owing to double-gene disruption of adrenoceptors that negatively regulate norepinephrine release, α 2A -AR, and α 2C -AR (α 2A/2C -AR −/− mice). As expected, T 3 treatment caused a generalized decrease in the areal bone mineral density (aBMD) of WT mice (determined by DEXA), followed by deleterious effects on the trabecular and cortical bone microstructural parameters (determined by μCT) of the femur and vertebra and on the biomechanical properties (maximum load, ultimate load, and stiffness) of the femur. Surprisingly, α 2A/2C -AR −/− mice were resistant to most of these T 3 -induced negative effects. Interestingly, the mRNA expression of osteoprotegerin, a protein that limits osteoclast activity, was upregulated and downregulated by T 3 in the bone of α 2A/2C -AR −/− and WT mice, respectively. β 1 -AR mRNA expression and IGF-I serum levels, which exert bone anabolic effects, were increased by T 3 treatment only in α 2A/2C -AR −/− mice. As expected, T 3 inhibited the cell growth of calvaria-derived osteoblasts isolated from WT mice, but this effect was abolished or reverted in cells isolated from KO mice. Collectively, these findings support the hypothesis of a TH-SNS interaction to control bone mass and structure of young adult mice and suggests that this interaction may involve α 2 -AR signaling. Finally, the present findings offer new insights into the mechanisms through which TH regulates bone mass, structure, and physiology." @default.
• W2114636153 created "2016-06-24" @default.
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• W2114636153 date "2014-08-15" @default.
• W2114636153 modified "2023-09-30" @default.
• W2114636153 title "Thyroid hormone interacts with the sympathetic nervous system to modulate bone mass and structure in young adult mice" @default.
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• W2114636153 doi "https://doi.org/10.1152/ajpendo.00643.2013" @default.
• W2114636153 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25005498" @default.
• W2114636153 hasPublicationYear "2014" @default.
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