These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Regulation of pituitary insulin-like growth factor-I messenger ribonucleic acid levels in rats harboring somatomammotropic tumors: implications for growth hormone autoregulation.
    Author: Fagin JA, Brown A, Melmed S.
    Journal: Endocrinology; 1988 May; 122(5):2204-10. PubMed ID: 3359980.
    Abstract:
    Insulin-like growth factor-I (IGF-I) is produced in multiple tissues and is believed to exert its action in a paracrine or autocrine fashion. We have investigated the GH dependency of tissue IGF-I gene expression in rats harboring implanted somatomammotropic tumors. Circulating GH and radioimmunoassayable IGF-I levels were markedly elevated in these animals. Hepatic IGF-I messenger RNA (mRNA) transcripts were induced about 5-fold in the tumor-bearing rats relative to control animals, and about 50-fold relative to the hypophysectomized liver IGF-I mRNA. IGF-I mRNA content was also modestly induced in the heart, muscle, and kidney of the tumor-bearing animals. IGF-I mRNA transcripts of 8.0, 6.2, 3.8, 2.4, 1.3, and 1.0 kilobases were markedly stimulated in the pituitaries of the GH-tumor bearing rats relative to control pituitaries. Pituitary IGF-I mRNA induction was maximal between 2 and 6 weeks after tumor implantation, a time at which circulating GH levels were also increasing sharply. As previously reported, pituitary GH mRNA was inhibited in tumor-bearing rats. The stimulation of pituitary IGF-I gene expression in these animals, therefore, appears to be dependent on circulating, and not local, pituitary GH concentrations. These data support the GH dependency of pituitary IGF-I gene expression. IGF-I is known to decrease GH production in vitro. High circulating levels of IGF-I present in these animals may account for the observed inhibition of GH gene expression. These data raise the alternative possibility that induction of locally produced IGF-I may contribute to this phenomenon.
    [Abstract] [Full Text] [Related] [New Search]