Fox J, Miller M A, Stroup G B, Nemeth E F, Miller S C
Department of Pharmacology, NPS Pharmaceuticals, Inc., Salt Lake City, UT 84108, USA.
Bone. 1997 Aug;21(2):163-9. doi: 10.1016/s8756-3282(97)00108-7.
Parathyroid hormone (PTH) administration increases bone mass in normal and osteopenic animals. However, this treatment currently requires the daily injection of large amounts of PTH, and the relationship of these doses to plasma levels of PTH that are achievable physiologically is unknown. We determined in ovariectomized (ovx) rats: 1) the plasma PTH levels that occur after the subcutaneous injection of graded doses of rat PTH, 2) whether similar PTH levels can be achieved by stimulation of endogenous PTH secretion, and 3) whether a plasma PTH profile that is achievable physiologically is anabolic on bone. Injection of 1, 5, or 25 micrograms/kg rat PTH-(1-34) increased plasma PTH by 46, 164, or 520 pg/mL, respectively, above basal levels within 60 min. Infusion of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid for 2 h reduced plasma Ca2+ by 0.36 mmol/L and produced a total plasma PTH response (area under the plasma PTH curve) similar to that with the 5 micrograms/kg rat PTH injection. Then, 1, 5, or 25 micrograms/kg doses of rat PTH-(1-34) were injected subcutaneously daily for 28 days in 19-week-old rats that were ovx 7 weeks earlier. The 5 and 25 micrograms/kg doses significantly increased bone mineral density in the distal femur and trabecular bone area and average trabecular thickness in the proximal tibia. All doses of PTH significantly increased indices of trabecular connectivity and cancellous bone formation, including double-labeled surface, mineralizing surface, and surface-referent bone formation rate. In conclusion, anabolic effects on bone can be achieved with a plasma PTH profile similar to that attained following stimulation of the parathyroid gland by induced hypocalcemia. These data suggest that agents that transiently increase endogenous PTH secretion may represent a novel means to promote anabolic effects in skeletal tissues.
给予甲状旁腺激素(PTH)可增加正常动物和骨质减少动物的骨量。然而,目前这种治疗需要每日注射大量的PTH,且这些剂量与生理上可达到的PTH血浆水平之间的关系尚不清楚。我们在去卵巢(ovx)大鼠中进行了以下研究:1)皮下注射不同剂量的大鼠PTH后出现的血浆PTH水平;2)通过刺激内源性PTH分泌是否能达到相似的PTH水平;3)生理上可达到的血浆PTH谱对骨骼是否具有合成代谢作用。注射1、5或25微克/千克大鼠PTH-(1-34)可使血浆PTH在60分钟内分别比基础水平升高46、164或520皮克/毫升。输注乙二醇双(β-氨基乙基醚)-N,N,N',N'-四乙酸2小时可使血浆Ca2+降低0.36毫摩尔/升,并产生与注射5微克/千克大鼠PTH相似的总血浆PTH反应(血浆PTH曲线下面积)。然后,在7周前进行卵巢切除的19周龄大鼠中,每日皮下注射1、5或25微克/千克剂量的大鼠PTH-(1-34),持续28天。5和25微克/千克剂量显著增加了股骨远端的骨矿物质密度、小梁骨面积以及胫骨近端的平均小梁厚度。所有剂量的PTH均显著增加了小梁连接性和松质骨形成的指标,包括双标记表面、矿化表面和表面参照骨形成率。总之,与低钙血症诱导刺激甲状旁腺后所达到的血浆PTH谱相似的情况下,对骨骼可产生合成代谢作用。这些数据表明,能短暂增加内源性PTH分泌的药物可能代表了一种促进骨骼组织合成代谢作用的新方法。