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

Shoshana Yakar, Jun L.I. Liu, Bethel Stannard, Andrew Butler, Domenici Accili, Brian Sauer, Derek Leroith

Research output: Contribution to journalArticlepeer-review

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

ASJC Scopus subject areas

  • General

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