Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 122, Issue 10, Pages 3737-3741Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI63948
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Funding
- NIH [DK080459, DK069713, DK052464, AG23186, DK70526]
- VA Merit Review Program
- USDA ARS CRIS Program [5450-51000-046-00D]
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The osteoporosis associated with human hyperthyroidism has traditionally been attributed to elevated thyroid hormone levels. There is evidence, however, that thyroid-stimulating hormone (TSH), which is low in most hyperthyroid states, directly affects the skeleton. Importantly, Tshr-knockout mice are osteopenic. In order to determine whether low TSH levels contribute to bone loss in hyperthyroidism, we compared the skeletal phenotypes of wild-type and Tshr-knockout mice that were rendered hyperthyroid. We found that hyperthyroid mice lacking TSHR had greater bone loss and resorption than hyperthyroid wild-type mice, thereby demonstrating that the absence of TSH signaling contributes to bone loss. Further, we identified a TSH-like factor that may confer osteoprotection. These studies suggest that therapeutic suppression of TSH to very low levels may contribute to bone loss in people.
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