Sun Li, Davies Terry F, Blair Harry C, Abe Etsuko, Zaidi Mone
Department of Medicine, Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY 10029, USA.
Ann N Y Acad Sci. 2006 Apr;1068:309-18. doi: 10.1196/annals.1346.033.
We have recently challenged the view that the bone loss associated with hyperthyroidism is solely due to elevated thyroid hormone levels. We find that thyroid-stimulating hormone (TSH), derived from the anterior pituitary gland, inhibits bone resorption by the osteoclast. Mice haploinsufficient in the TSH receptor show reduced bone density and evidence of enhanced bone resorption in the face of normal thyroid function. In humans, TSH inhibits markers of bone resorption with a single administration, and low TSH levels correlate with increased fracture risk. The evidence that low TSH levels predispose to osteoporosis in hyperthyroidism is discussed in view of the emerging role of pituitary hormones in bone biology.
我们最近对一种观点提出了质疑,即与甲状腺功能亢进相关的骨质流失完全是由于甲状腺激素水平升高所致。我们发现,源自垂体前叶的促甲状腺激素(TSH)可抑制破骨细胞的骨吸收。促甲状腺激素受体单倍体不足的小鼠骨密度降低,且在甲状腺功能正常的情况下有骨吸收增强的迹象。在人类中,单次给予促甲状腺激素可抑制骨吸收标志物,促甲状腺激素水平低与骨折风险增加相关。鉴于垂体激素在骨生物学中的新作用,我们讨论了促甲状腺激素水平低易导致甲状腺功能亢进患者患骨质疏松症的证据。