The Somatomedin Hypothesis: 2001
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ID: 296139
2001
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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 liverspecific 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.
| Reference Key |
openalex_W2102303758
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| Authors | Derek Le Roith, Carolyn A. Bondy, Shoshana Yakar, Jun‐Li Liu, Andrew A. Butler |
| Journal | endocrine reviews |
| Year | 2001 |
| DOI |
10.1210/edrv.22.1.0419
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| URL | |
| Keywords | Keywords not found |
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