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Treatment of Ligament Constructs with Exercise-conditioned Serum: A Translational Tissue Engineering Model
Published on: June 11, 2017
Serum IGF-1 affects skeletal acquisition in a temporal and compartment-specific manner
Hayden-William Courtland1, Sebastien Elis, Yingjie Wu
1Division of Endocrinology, Diabetes and Bone Disease, Mount Sinai School of Medicine, New York, New York, United States of America.
Plos One
|March 30, 2011
Summary
Serum Insulin-like Growth Factor-1 (IGF-1) is crucial for bone accrual during growth. Depleting IGF-1 after peak bone mass enhances trabecular bone but does not harm cortical bone in adult mice.
Area of Science:
- Endocrinology
- Bone Biology
- Skeletal Physiology
Background:
- Insulin-like Growth Factor-1 (IGF-1) is vital for skeletal development and bone mass maintenance.
- Decreased serum IGF-1 levels correlate with reduced bone mineral density (BMD) in aging.
- Previous mouse models could not isolate the timing of IGF-1's skeletal effects.
Purpose of the Study:
- To investigate the temporal effects of IGF-1 depletion on skeletal compartments.
- To characterize the skeletal changes in inducible IGF-1 deficient (iLID) mice at different ages.
- To determine if IGF-1 is essential for maintaining bone mass after peak acquisition.
Main Methods:
- Skeletal characterization of inducible LID (iLID) mice with IGF-1 depletion at selected ages.
- Analysis of trabecular and cortical bone properties at various time points.
- Comparison of bone parameters between iLID mice and control groups.
Main Results:
- IGF-1 depletion before adulthood (4 weeks) impaired trabecular and cortical bone in male mice.
- IGF-1 depletion at 8 weeks reduced cortical bone properties but not trabecular bone in late adulthood.
- IGF-1 depletion after peak bone acquisition (16 weeks) improved trabecular bone without affecting cortical bone.
Conclusions:
- Serum IGF-1 is essential for bone accrual during postnatal growth.
- Post-peak bone acquisition, IGF-1 depletion has compartment-specific effects.
- IGF-1 is not detrimental to cortical bone mass in older adult mice after peak acquisition.
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