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Am J Physiol Regul Integr Comp Physiol 271: R1632-R1637, 1996;
0363-6119/96 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 271, Issue 6 1632-R1637, Copyright © 1996 by American Physiological Society


ARTICLES

Intravenous infusion of insulin-like growth factor I in fetal sheep reduces hepatic IGF-I and IGF-II mRNAs

K. L. Kind, J. A. Owens, F. Lok, J. S. Robinson, K. J. Quinn, L. Mundy, R. S. Gilmour and P. C. Owens
Department of Obstetrics and Gynaecology, University of Adelaide, Australia.

Liver contains the highest concentrations of insulin-like growth factor (IGF) I mRNA in adult rats and sheep and is a major source of circulating IGF-I. In rats, inhibition of hepatic IGF-I production by exogenous IGF-I has been reported. In fetal sheep, skeletal muscle and liver are major sites of IGF-I synthesis and potential sources of circulating IGF-I. To determine whether feedback inhibition of IGF gene expression in fetal liver or muscle by IGF-I occurs, IGF-I and IGF-II mRNAs were measured in these tissues after intravenous infusion of recombinant human IGF-I into fetal sheep. Infusion of IGF-I (26 +/- 4 micrograms.h-1.kg-1; n = 6) or saline (n = 6) commenced on day 120 of pregnancy (term = 150 days) and continued for 10 days. Plasma concentrations of IGF-I were threefold higher in infused fetuses at 130 days of gestation (P < 0.0003), whereas those of IGF-II were unchanged. IGF-I infusion reduced the relative abundance of IGF-I mRNA (P < 0.0002) and IGF-II mRNA (P < 0.01) in fetal liver by approximately 50% but did not alter IGF-I or IGF-II mRNA in skeletal muscle. These results indicate that IGF-I inhibits the expression of both IGF-I and IGF-II genes in fetal liver and that IGF gene expression in fetal liver and muscle is differentially regulated by IGF-I.


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Am. J. Physiol. Endocrinol. Metab.Home page
F. H. Bloomfield, M. K. Bauer, P. L. Van Zijl, P. D. Gluckman, and J. E. Harding
Amniotic IGF-I supplements improve gut growth but reduce circulating IGF-I in growth-restricted fetal sheep
Am J Physiol Endocrinol Metab, February 1, 2002; 282(2): E259 - E269.
[Abstract] [Full Text] [PDF]




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