Normal growth and development in the absence of hepatic insulin-like growth factor

Shoshana Yakar, J. L. Liu, B. Stannard, A. Butler, D. Accili, B. Sauer, D. LeRoith

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)7324-7329
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume96
Issue number13
DOIs
StatePublished - Jun 22 1999

Fingerprint

Somatomedins
Insulin-Like Growth Factor I
Growth and Development
Liver
Gene Deletion
Growth
Thigh
Genetic Recombination
Growth Hormone
Body Weight
Messenger RNA
Genes

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Normal growth and development in the absence of hepatic insulin-like growth factor. / Yakar, Shoshana; Liu, J. L.; Stannard, B.; Butler, A.; Accili, D.; Sauer, B.; LeRoith, D.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 96, No. 13, 22.06.1999, p. 7324-7329.

Research output: Contribution to journalArticle

Yakar, Shoshana ; Liu, J. L. ; Stannard, B. ; Butler, A. ; Accili, D. ; Sauer, B. ; LeRoith, D. / Normal growth and development in the absence of hepatic insulin-like growth factor. In: Proceedings of the National Academy of Sciences of the United States of America. 1999 ; Vol. 96, No. 13. pp. 7324-7329.
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