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|Title:||Intravenous infusion of insulin-like growth factor I in fetal sheep reduces hepatic IGF-I and IGF-II mRNAs|
|Citation:||American Journal of Physiology, 1996; 271(6):R1632-R1637|
|Publisher:||American Physiological Society|
|Karen L. Kind, Julie A. Owens, Fong, Lok, Jeffrey S. Robinson, Kirsty J. Quinn, Linda Mundy, R. Stewart Gilmour, and Phillip C. Owens|
|Abstract:||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.|
Insulin-Like Growth Factor I
Insulin-Like Growth Factor II
Insulin-Like Growth Factor Binding Proteins
|Rights:||Copyright © 1996 the American Physiological Society|
|Appears in Collections:||Aurora harvest 4|
Obstetrics and Gynaecology publications
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