Oldham S B, Gruber H E, Rude R K
University of Southern California, School of Medicine, Los Angeles 90033.
Osteoporos Int. 1992 Jul;2(4):174-9. doi: 10.1007/BF01623923.
Both estrogen and androgen have been reported to attenuate cyclic AMP responses to parathyroid hormone stimulation in cultured bone cells. The present study examines the effect of in vivo estrogen deficiency on skeletal adenylate cyclase (AC) activity. The AC activity was compared in bone membranes prepared from normal female guinea pigs and from age-matched guinea pigs 3 weeks after ovariectomy. Histomorphometric analysis of femoral specimens from the ovariectomized guinea pigs demonstrated significant decreases in percentage bone volume, the percentage eroded surfaces and osteoclast numbers, and increased osteoid thickness, compared with the normal controls. No differences were found in basal AC activity, the ability of bone AC to be stimulated by parathyroid hormone (bPTH(1-34)) or isoproterenol, or in the regulation of AC activity by calcium and magnesium. We conclude that bone AC is not a direct target for estrogen effects on bone cells and that the reported effects of sex steroids on cAMP levels in bone cells probably act via an indirect mechanism.
据报道，雌激素和雄激素均可减弱培养骨细胞中甲状旁腺激素刺激引起的环磷酸腺苷反应。本研究检测了体内雌激素缺乏对骨骼腺苷酸环化酶（AC）活性的影响。比较了正常雌性豚鼠和卵巢切除术后3周的年龄匹配豚鼠制备的骨膜中的AC活性。与正常对照组相比，卵巢切除豚鼠股骨标本的组织形态计量学分析显示骨体积百分比、侵蚀表面百分比和破骨细胞数量显著降低，类骨质厚度增加。在基础AC活性、骨AC受甲状旁腺激素（bPTH(1-34)）或异丙肾上腺素刺激的能力，或钙和镁对AC活性的调节方面未发现差异。我们得出结论，骨AC不是雌激素对骨细胞作用的直接靶点，并且性类固醇对骨细胞中环磷酸腺苷水平的报道作用可能通过间接机制起作用。
