Effect of dexamethasone on insulin-like growth factor-1 expression in a rabbit model of growth retardation

Background/Purpose: The maternal administration of steroids promotes fetal maturative effects in the gastrointestinal tract. To determine if fetal ins ulin-like growth factor-1 (IGF-1) expression is altered in response to mate rnal dexamethasone administration, this rabbit model of intrauterine growth retardation (IUGR)was utilized. Methods: Eight pregnant rabbits received either dexamethasone (Dex 0.1 mg/k g/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 f avored (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 reac tion (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 pro tein 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 De xRunt 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 prote in 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-ret arded fetus appears to be particularly responsive. Copyright (C) 2000 by W. B. Saunders Company.