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Related Experiment Videos

The somatomedin hypothesis: 2001.

D Le Roith1, C Bondy, S Yakar

  • 1Clinical Endocrinology Branch, National Institutes of Health, Bethesda, Maryland 20892-1758, USA. derek@helix.nih.gov

Endocrine Reviews
|February 13, 2001
PubMed
Summary
This summary is machine-generated.

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Normal growth in mice lacking liver-produced insulin-like growth factor-I (IGF-I) suggests other sources contribute to development. Further research is needed to clarify the role of local IGF-I signaling.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Genetics

Background:

  • The original somatomedin hypothesis proposed pituitary GH controls growth via liver-produced IGF-I.
  • Discoveries indicate IGF-I is produced by most tissues, leading to debate on autocrine/paracrine vs. circulating IGF-I roles.
  • Transgenic and gene-deletion technologies are used to investigate IGF-I functions.

Purpose of the Study:

  • To investigate the role of liver-derived insulin-like growth factor-I (IGF-I) in postnatal growth and development.
  • To differentiate the contributions of circulating IGF-I versus locally produced IGF-I.

Main Methods:

  • Utilized a liver-specific igf-1 gene-deleted mouse model.
  • Analyzed postnatal growth and development parameters.

Related Experiment Videos

  • Measured circulating and free IGF-I levels, as well as IGF-binding protein levels.
  • Main Results:

    • Mice with liver-specific igf-1 deletion exhibited normal postnatal growth and development.
    • Circulating IGF-I and IGF-binding protein levels were markedly reduced.
    • Free IGF-I levels remained normal in these mice.

    Conclusions:

    • Normal growth in the absence of liver-derived IGF-I suggests alternative sources of free IGF-I are sufficient for postnatal development.
    • The precise contribution of autocrine/paracrine IGF-I signaling to overall growth requires further investigation.