Expression of insulin-like growth factor i in transgenic mice with elevated levels of growth hormone is correlated with growth

L. S. Mathews, Robert E Hammer, R. L. Brinster, R. D. Palmiter

Research output: Contribution to journalArticlepeer-review

138 Scopus citations

Abstract

To study the role of insulin-like growth factor I (IGF-I) in mediating the growth-promoting function of GH, IGF-I expression was assayed in transgenic mice carrying either GH or GRF fusion genes. These mice exhibit enhanced growth as a result of high level ectopic expression of GH and have 2-fold elevation of both hepatic IGF-I mRNA levels and circulating IGF-I levels. Hepatic IGF-I mRNA levels are low at birth regardless of GH levels; they increase approximately 10-fold during postnatal development and become GH inducible 2 weeks after birth. The ontogeny of circulating IGF-I is similar. Accelerated growth in transgenic mice with GH fusion genes commences 3 weeks after birth despite high circulating GH levels at least as early as birth. In addition, endogenous mouse GH-secreting somatotroph cells in the pituitary are present in normal numbers at 3 weeks, but are undetectable 4 weeks after birth. Because the time at which IGF-I expression becomes GH responsive slightly precedes both the initiation of accelerated growth and the time when endogenous GH disappears, we conclude that IGF-I is directly involved in mediating the GH signal and that delayed induction of IGF-I gene expression is responsible, at least in part, for the delayed onset of other GH-responsive events.

Original languageEnglish (US)
Pages (from-to)433-437
Number of pages5
JournalEndocrinology
Volume123
Issue number1
DOIs
StatePublished - Jul 1 1988

ASJC Scopus subject areas

  • Endocrinology

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