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生长激素可预防循环中胰岛素样生长因子 (IGF-1) 水平低所致的去卵巢引起的骨丢失。

Growth hormone protects against ovariectomy-induced bone loss in states of low circulating insulin-like growth factor (IGF-1).

机构信息

Leni & Peter W. May Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY 10029, USA.

出版信息

J Bone Miner Res. 2010 Feb;25(2):235-46. doi: 10.1359/jbmr.090723.

DOI:10.1359/jbmr.090723
PMID:19619004
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3153382/
Abstract

Early after estrogen loss in postmenopausal women and ovariectomy (OVX) of animals, accelerated endosteal bone resorption leads to marrow expansion of long bone shafts that reduce mechanical integrity. Both growth hormone (GH) and insulin-like growth factor (IGF-1) are potent regulators of bone remodeling processes. To investigate the role of the GH/IGF-1 axis with estrogen deficiency, we used the liver IGF-1-deficient (LID) mouse. Contrary to deficits in controls, OVX of LID mice resulted in maintenance of cortical bone mechanical integrity primarily owing to an enhanced periosteal expansion affect on cross-sectional structure (total area and cortical width). The serum balance in LID that favors GH over IGF-1 diminished the effects of ablated ovarian function on numbers of osteoclast precursors in the marrow and viability of osteocytes within the cortical matrix and led to less endosteal resorption in addition to greater periosteal bone formation. Interactions between estrogen and the GH/IGF-1 system as related to bone remodeling provide a pathway to minimize degeneration of bone tissue structure and osteoporotic fracture.

摘要

绝经后妇女和动物卵巢切除(OVX)后早期,骨内骨吸收加速导致长骨干骨髓扩张,从而降低机械完整性。生长激素(GH)和胰岛素样生长因子(IGF-1)是骨重塑过程的强大调节剂。为了研究 GH/IGF-1 轴与雌激素缺乏的关系,我们使用了肝脏 IGF-1 缺乏(LID)小鼠。与对照组的缺陷相反,LID 小鼠的 OVX 导致皮质骨机械完整性得以维持,主要归因于对横截面结构(总面积和皮质宽度)的增强骨膜扩张作用。LID 中有利于 GH 而不是 IGF-1 的血清平衡减弱了卵巢功能切除对骨髓中破骨细胞前体数量和皮质基质中骨细胞活力的影响,导致骨内吸收减少,骨膜形成增加。雌激素与 GH/IGF-1 系统之间的相互作用与骨重塑有关,为最小化骨组织结构退化和骨质疏松性骨折提供了途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/01c24eb98c95/jbmr0025-0235-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/eb39911f1b0c/jbmr0025-0235-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/96e94a495a45/jbmr0025-0235-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/f252d4e6209a/jbmr0025-0235-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/04c598b79a74/jbmr0025-0235-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/01c24eb98c95/jbmr0025-0235-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/eb39911f1b0c/jbmr0025-0235-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/838c8cffc862/jbmr0025-0235-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/4f7cf29128bc/jbmr0025-0235-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/96e94a495a45/jbmr0025-0235-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/f252d4e6209a/jbmr0025-0235-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/04c598b79a74/jbmr0025-0235-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5b6/3153382/01c24eb98c95/jbmr0025-0235-f7.jpg

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