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The Somatomedin Hypothesis: 2001

Le Roith, Derek, Bondy, Carolyn, Yakar, Shoshana, Liu, Jun-Li, Butler, Andrew·2001·Endocrine Reviews

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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Research works printed but not linked: 37

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Metadata

Authors
Le Roith, D., Bondy, C., Yakar, S., Liu, J.-L., & Butler, A.
Venue
Endocrine Reviews
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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CoChat. (2026). Citation check: The Somatomedin Hypothesis: 2001. https://app.cochat.ai/papers/10.1210/edrv.22.1.0419
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Le Roith, D., Bondy, C., Yakar, S., Liu, J.-L., & Butler, A. (2001). The Somatomedin Hypothesis: 2001. Endocrine Reviews. https://doi.org/10.1210/edrv.22.1.0419

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