BACKGROUND/ PURPOSE: The maternal administration of steroids promotes fetal maturative effects in the gastrointestinal tract. To determine if fetal insulin-like growth factor-1 (IGF-1) expression is altered in response to maternal dexamethasone administration, this rabbit model of intrauterine growth retardation (IUGR) was utilized. METHODS: Eight pregnant rabbits received either dexamethasone (Dex 0.1 mg/kg/d intramuscular), or normal saline (Cont) on gestational days 26 and 27. Fetuses were harvested on gestational day 28 or 29 and were identified as favored (Fav) or runt (Runt): DexFav, DexRunt, ContFav, and ContRunt. Fetal weight was recorded and the serum, amniotic fluid, liver, kidney, and small intestine (SI) were collected. Reverse transcription polymerase chain reaction (RT-PCR) was used to measure IGF-1/beta-actin mRNA densitometric band ratios in all tissues. Radioimmunoassay (RIA) was used to measure IGF-1 protein levels in the serum and amniotic fluid. RESULTS: Weight was decreased in the Runt fetuses at all time-points (P < .08). The percent weight accretion from day 28 to 29, was greatest in the DexRunt fetus (P < .001), suggesting "catch-up" growth. All Dex fetuses (Fav and Runt) had increased liver and proximal, middle and distal SI IGF-1 mRNA at day 28 and elevated levels in the liver, proximal and distal SI at day 29 compared with control fetuses. The DexRunt fetuses had serum IGF-1 protein surpassing that of the DexFav fetus at day 28. CONCLUSIONS: This report provides the first description of maternal steroid administration effecting a marked increase in fetal IGF-1 mRNA expression and IGF-1 protein levels in an in vivo rabbit model of IUGR. The growth-retarded fetus appears to be particularly responsive.
BACKGROUND/ PURPOSE: The maternal administration of steroids promotes fetal maturative effects in the gastrointestinal tract. To determine if fetal insulin-like growth factor-1 (IGF-1) expression is altered in response to maternal dexamethasone administration, this rabbit model of intrauterine growth retardation (IUGR) was utilized. METHODS: Eight pregnant rabbits received either dexamethasone (Dex 0.1 mg/kg/d intramuscular), or normal saline (Cont) on gestational days 26 and 27. Fetuses were harvested on gestational day 28 or 29 and were identified as favored (Fav) or runt (Runt): DexFav, DexRunt, ContFav, and ContRunt. Fetal weight was recorded and the serum, amniotic fluid, liver, kidney, and small intestine (SI) were collected. Reverse transcription polymerase chain reaction (RT-PCR) was used to measure IGF-1/beta-actin mRNA densitometric band ratios in all tissues. Radioimmunoassay (RIA) was used to measure IGF-1 protein levels in the serum and amniotic fluid. RESULTS: Weight was decreased in the Runt fetuses at all time-points (P < .08). The percent weight accretion from day 28 to 29, was greatest in the DexRunt fetus (P < .001), suggesting "catch-up" growth. All Dex fetuses (Fav and Runt) had increased liver and proximal, middle and distal SI IGF-1 mRNA at day 28 and elevated levels in the liver, proximal and distal SI at day 29 compared with control fetuses. The DexRunt fetuses had serum IGF-1 protein surpassing that of the DexFav fetus at day 28. CONCLUSIONS: This report provides the first description of maternal steroid administration effecting a marked increase in fetal IGF-1 mRNA expression and IGF-1 protein levels in an in vivo rabbit model of IUGR. The growth-retarded fetus appears to be particularly responsive.
Authors: Kathryn L Gatford; Julie A Owens; Shaofu Li; Timothy J M Moss; John P Newnham; John R G Challis; Deborah M Sloboda Journal: Am J Physiol Endocrinol Metab Date: 2008-05-20 Impact factor: 4.310
Authors: Jorge Lopez-Tello; Maria Arias-Alvarez; Maria Angeles Jimenez-Martinez; Rosa Maria Garcia-Garcia; Maria Rodriguez; Pedro Luis Lorenzo Gonzalez; Ruben Bermejo-Poza; Antonio Gonzalez-Bulnes; Pilar Garcia Rebollar Journal: PLoS One Date: 2017-01-03 Impact factor: 3.240