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Updated: Jul 23, 2026
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A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
Published on: April 28, 2016
The somatomedin hypothesis: 2001
1Clinical Endocrinology Branch, National Institutes of Health, Bethesda, Maryland 20892-1758, USA. derek@helix.nih.gov
Endocrine Reviews
|February 13, 2001
Summary
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.
- 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.
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