Ontogeny of insulin-like growth factor 1 in a rabbit model of growth retardation.

摘要: Many cases of intrauterine growth retardation (IUGR) result from placental insufficiency, but the molecular signals accompanying this event are unknown. Insulin-like factor 1 (IGF-1) is a potent mitogen for fetal tissues and lowered in serum human infants with IUGR. The rabbit provides an optimal model study IUGR based on position. To determine if IGF-1 expression altered growth-retarded fetus, naturally occurring was used. Four pairs were harvested Days 21, 23, 25, 27, 29, 31 their normal 31-day gestation; they identified uterine position as or retarded. Fetal weight recorded serum, amniotic fluid, liver, kidney, small intestine (SI) collected. SI divided into three equal segments: proximal, middle, distal. Reverse transcription polymerase chain reaction (RT-PCR) used to measure IGF-1/β-actin mRNA densitometric band ratios all tissues. Radioimmunoassay (RIA) protein levels fluid. Statistical analysis performed using ANOVA paired Student's t test. Weights decreased fetuses at time points (P < 0.05), further validating Liver, distal during late gestation 0.01). Kidney increased throughout Compared counterparts, had trend toward points, reaching significance liver Day 27 = 0.002). Serum 0.05). fetuses, lower 0.02). Amniotic fluid than though not quite significance. rabbits depressed intestinal protein. correlate change. Further studies potential manipulation warranted investigate prenatal intervention treatment