Deakin University
Browse

Liver-derived IGF-I regulates cortical bone mass but is dispensable for the osteogenic response to mechanical loading in female mice

Download (318.86 kB)
Version 2 2024-06-05, 10:25
Version 1 2021-05-19, 10:58
journal contribution
posted on 2024-06-05, 10:25 authored by J Svensson, SH Windahl, Leanne SaxonLeanne Saxon, K Sjögren, A Koskela, J Tuukkanen, C Ohlsson
Low circulating IGF-I is associated with increased fracture risk. Conditional depletion of IGF-I produced in osteoblasts or osteocytes inhibits the bone anabolic effect of mechanical loading. Here, we determined the role of endocrine IGF-I for the osteogenic response to mechanical loading in young adult and old female mice with adult, liver-specific IGF-I inactivation (LI-IGF-I−/− mice, serum IGF-I reduced by ≈70%) and control mice. The right tibia was subjected to short periods of axial cyclic compressive loading three times/wk for 2 wk, and measurements were performed using microcomputed tomography and mechanical testing by three-point bending. In the nonloaded left tibia, the LI-IGF-I−/− mice had lower cortical bone area and increased cortical porosity, resulting in reduced bone mechanical strength compared with the controls. Mechanical loading induced a similar response in LI-IGF-I−/− and control mice in terms of cortical bone area and trabecular bone volume fraction. In fact, mechanical loading produced a more marked increase in cortical bone mechanical strength, which was associated with a less marked increase in cortical porosity, in the LI-IGF-I−/− mice compared with the control mice. In conclusion, liver-derived IGF-I regulates cortical bone mass, cortical porosity, and mechanical strength under normal (nonloaded) conditions. However, despite an ∼70% reduction in circulating IGF-I, the osteogenic response to mechanical loading was not attenuated in the LI-IGF-I−/− mice.

History

Journal

American journal of physiology: endocrinology and metabolism

Volume

311

Pagination

E138-E144

Location

Bethesda, Md.

Open access

  • Yes

ISSN

0193-1849

eISSN

1522-1555

Language

eng

Publication classification

C1.1 Refereed article in a scholarly journal, C Journal article

Issue

1

Publisher

American Physiological Society

Usage metrics

    Research Publications

    Categories

    No categories selected

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC