Thyroid Research Unit and The Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, and James J. Peters VA Medical Center, New York, New York 10029, USA.
J Clin Invest. 2012 Oct;122(10):3737-41. doi: 10.1172/JCI63948. Epub 2012 Sep 17.
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.
与人类甲状腺功能亢进相关的骨质疏松症传统上归因于甲状腺激素水平升高。然而，有证据表明，甲状腺刺激激素（TSH）在大多数甲状腺功能亢进状态下较低，直接影响骨骼。重要的是，TSHr 敲除小鼠呈骨质疏松症。为了确定低 TSH 水平是否导致甲状腺功能亢进中的骨丢失，我们比较了甲状腺功能亢进的野生型和 Tshr 敲除小鼠的骨骼表型。我们发现，缺乏 TSHR 的甲状腺功能亢进小鼠的骨丢失和吸收比甲状腺功能亢进野生型小鼠更严重，从而表明 TSH 信号缺失会导致骨丢失。此外，我们还发现了一种可能具有护骨作用的 TSH 样因子。这些研究表明，将 TSH 抑制到非常低的水平可能会导致人类的骨丢失。
