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Skeletal unloading induces resistance to insulin-like growth factor IIn previous studies with a hindlimb elevation model, we demonstrated that skeletal unloading transiently inhibits bone formation. This effect is limited to the unloaded bones (the normally loaded humerus does not cease growing), suggesting that local factors are of prime importance. IGF-I is one such factor; it is produced in bone and stimulates bone formation. To determine the impact of skeletal unloading on IGF-I production and function, we assessed the mRNA levels of IGF-I and its receptor (IGF-IR) in the proximal tibia and distal femur of growing rats during 2 weeks of hindlimb elevation. The mRNA levels for IGF-I and IGF-IR rose during hindlimb elevation, returning toward control values during recovery. This was accompanied by a 77% increase in IGF-I levels in the bone, peaking at day 10 of unloading. Changes in IGF binding protein levels were not observed. Infusion of IGF-I (200 micrograms/day) during 1 week of hindlimb elevation doubled the increase in bone mass of the control animals but failed to reverse the cessation of bone growth in the hindlimb-elevated animals. We conclude that skeletal unloading induces resistance to IGF-I, which may result secondarily in increased local production of IGF-I.
Document ID
20050000297
Acquisition Source
Ames Research Center
Document Type
Reprint (Version printed in journal)
Authors
Bikle, D. D.
(Veterans Administration Medical Center San Francisco, California)
Harris, J.
Halloran, B. P.
Morey-Holton, E. R.
Date Acquired
August 22, 2013
Publication Date
November 1, 1994
Publication Information
Publication: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
Volume: 9
Issue: 11
ISSN: 0884-0431
Subject Category
Life Sciences (General)
Distribution Limits
Public
Copyright
Other
Keywords
NASA Center ARC
NASA Discipline Musculoskeletal
Non-NASA Center

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