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The Somatomedin Hypothesis: 2001
Abstract
Since the original somatomedin hypothesis was conceived, a number of important discoveries have allowed investigators to modify the concept. Originally somatic growth was thought to be controlled by pituitary GH and mediated by circulating insulin-like growth factor-I (IGF-I, somatomedin C) expressed exclusively by the liver. With the discovery that IGF-I is produced by most, if not all, tissues, the role of autocrine/paracrine IGF-I vs. the circulating form has been hotly debated. Recent experiments using transgenic and gene-deletion technologies have attempted to answer these questions. In the liver-specific igf-1 gene-deleted mouse model, postnatal growth and development are normal despite the marked reduction in circulating IGF-I and IGF-binding protein levels; free IGF-I levels are normal. Thus, the normal postnatal growth and development in these animals may be due to normal free IGF-I levels (from as yet unidentified sources), although the role of autocrine/paracrine IGF-I has yet to be determined.
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Metadata
- Authors
- Le Roith, D., Bondy, C., Yakar, S., Liu, J.-L., & Butler, A.
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 2001-02-01
- Volume
- 22
- Issue
- 1
- Pages
- 53-74
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- OpenAlex
- W2102303758
- Cited by
- 1,257
- References
- 188
- FWCI
- 41.68
- Type
- journal article
- Language
- en
- Open access
- closed
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