胰淀素对培养的新生小鼠颅骨基础和甲状旁腺激素刺激的骨吸收的抑制作用。

Inhibitory effect of amylin on basal and parathyroid hormone-stimulated bone resorption in cultured neonatal mouse calvaria.

作者信息

Pietschmann P, Farsoudi K H, Hoffmann O, Klaushofer K, Hörandner H, Peterlik M

机构信息

Department of General and Experimental Pathology, University of Vienna Medical School, Austria.

出版信息

Bone. 1993 Mar-Apr;14(2):167-72. doi: 10.1016/8756-3282(93)90244-5.

DOI:10.1016/8756-3282(93)90244-5

PMID:8334035

Abstract

Amylin is a secretory product of pancreatic beta-cells which shares major sequence homology with calcitonin gene-related peptide. In neonatal mouse calvaria maintained in organ culture for 72 h, amylin inhibited basal (i.e., unstimulated) resorption in medium concentrations above 2.5 x 10(-9) M. In addition, amylin (> or = 1.0 x 10(-7) M) in a calcitonin-like fashion transiently inhibited bone resorption induced by 1.0 x 10(-8) M PTH ("escape phenomenon"). Pretreatment of calvarial bones with amylin (1.0 x 10(-8) - 1.0 x 10(-6) M) for 72 h attenuated the subsequent response to 1.0 x 10(-8) M PTH. Changes in location and appearance of osteoclasts in amylin-treated bones, as visualized by light microscopy, suggest that amylin inhibits bone resorption by causing a loss of specialized contact zones to the mineralized matrix in resorbing osteoclasts, and in addition, by preventing retraction of osteoblasts from the mineralized surface which impedes attachment of osteoclasts thereon.

摘要

胰淀素是胰腺β细胞的一种分泌产物，它与降钙素基因相关肽具有主要的序列同源性。在器官培养中维持72小时的新生小鼠颅骨中，胰淀素在浓度高于2.5×10⁻⁹M时抑制基础（即未刺激的）骨吸收。此外，胰淀素（≥1.0×10⁻⁷M）以类似降钙素的方式短暂抑制由1.0×10⁻⁸M甲状旁腺激素诱导的骨吸收（“逃逸现象”）。用胰淀素（1.0×10⁻⁸ - 1.0×10⁻⁶M）预处理颅骨72小时可减弱随后对1.0×10⁻⁸M甲状旁腺激素的反应。通过光学显微镜观察，在经胰淀素处理的骨骼中破骨细胞的位置和外观变化表明，胰淀素通过导致正在吸收的破骨细胞与矿化基质的特殊接触区丧失来抑制骨吸收，此外，还通过阻止成骨细胞从矿化表面退缩来抑制骨吸收，而成骨细胞的退缩会阻碍破骨细胞在其上的附着。