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Normal growth and development in the absence of hepatic insulin-like growth factor I
Open accessAbstract
The somatomedin hypothesis proposed that insulin-like growth factor I (IGF-I) was a hepatically derived circulating mediator of growth hormone and is a crucial factor for postnatal growth and development. To reassess this hypothesis, we have used the Cre/ loxP recombination system to delete the igf1 gene exclusively in the liver. igf1 gene deletion in the liver abrogated expression of igf1 mRNA and caused a dramatic reduction in circulating IGF-I levels. However, growth as determined by body weight, body length, and femoral length did not differ from wild-type littermates. Although our model proves that hepatic IGF-I is indeed the major contributor to circulating IGF-I levels in mice it challenges the concept that circulating IGF-I is crucial for normal postnatal growth. Rather, our model provides direct evidence for the importance of the autocrine/paracrine role of IGF-I.
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Metadata
- Authors
- Yakar, S., Liu, J.-L., Stannard, B., Butler, A., Accili, D., Sauer, B., & LeRoith, D.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-06-22
- Volume
- 96
- Issue
- 13
- Pages
- 7324-7329
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2054121324
- Cited by
- 1,420
- References
- 0
- FWCI
- 46.81
- Type
- journal article
- Language
- en
- Open access
- green
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