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Title: Androgens inhibit the osteogenic response to mechanical loading in adult male mice
Authors: Sinnesael, Mieke
Laurent, Michaƫl
Jardi, Ferran
Dubois, Vanessa
Deboel, Ludo
Delisser, Peter
Behets, Geert J
D'Haese, Patrick C
Carmeliet, Geert
Claessens, Frank
Vanderschueren, Dirk # ×
Issue Date: Apr-2015
Publisher: Association for the Study of Internal Secretions
Series Title: Endocrinology vol:156 issue:4 pages:1343-53
Abstract: Androgens are well known to enhance exercise-induced muscle hypertrophy, however whether androgens also influence bone's adapative response to mechanical loading remains unclear. We studied the adaptive osteogenic response to unilateral in vivo mechanical loading of tibia in adult male mice in both a long and a short term experimental set-up. Mice were divided in 4 groups: sham-operated, orchidectomized (ORX), testosterone (ORX+T) or non-aromatizable dihydrotestosterone (ORX+DHT) replacement. Significant interactions between androgen status and osteogenic response to mechanical loading were observed. Cortical thickness increased by T (0.14 vs. 0.11 mm sham, p<0.05) and DHT (0.17 vs. 0.11 mm sham, p<0.05). However, T partially (+36%) and DHT completely (+10%) failed to exhibit the loading-related increase observed in sham (+107%) and ORX (+131%, all p<0.05) mice. ORX decreased periosteal bone formation (PsBFR), which was restored to sham levels by T and DHT. However, both androgens completely suppressed the loading-related increase in PsBFR. Short term loading decreased the number of sclerostin positive osteocytes in sham, whereas in control fibulas, ORX decreased and T increased the number of sclerostin positive osteocytes. Loading no longer downregulated sclerostin in ORX or T groups. In conclusion, both T and DHT suppress the osteogenic response to mechanical loading.
ISSN: 0013-7227
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Clinical and Experimental Endocrinology
Gerontology and Geriatrics
Laboratory of Molecular Endocrinology
× corresponding author
# (joint) last author

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