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Growth hormone protects against ovariectomy‐induced bone loss in states of low circulating insulin‐like growth factor (IGF‐1)
Author(s) -
Fritton J Christopher,
Emerton Kelly B,
Sun Hui,
Kawashima Yuki,
Mejia Wilson,
Wu Yingjie,
Rosen Clifford J,
Panus David,
Bouxsein Mary,
Majeska Robert J,
Schaffler Mitchell B,
Yakar Shoshana
Publication year - 2010
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.090723
Subject(s) - endocrinology , insulin like growth factor , medicine , growth factor , growth hormone , hormone , insulin , receptor
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. © 2010 American Society for Bone and Mineral Research