Correlational Study On Expression Of IGF-2and PGC-1α In IUGR Rats

Objective To explore expression changes of insulin-like Growth factor-2(IGF-2),phos-phoinositide3-kinase(PI3K), serine/threonine-protein kinases(AKT2),peroxisome proli-ferator-activated receptor-γ coactivator-1α(PGC-1α)in liver and placenta tissues ofintrauterine growth retardation rats with catch-up growth (CG-IUGR) for the purpose ofelucidating potential mechanism of insulin resistance in CG-IUGR offspring.Methods We established a CG-IUGR rats models with maternal nutritional restrictionduring the whole pregnant period and reducing the litter size of IUGR offspring after birth.The mRNA levels of IGF-2in placenta and liver tissues were detected via Real-time PCRrespectively and protein expression changes of PI3K,AKT2and PGC-1α were alsoevaluated by western blot. Besides, plasma was also isolated from IUGR and untreated SDrats of8weeks to detect triglyceride(TG)levels, which have a strong positive correlationwith metabolic syndrome, and fatty degeneration was observed in liver tissues via HE andOil red O staining.Results IGF2mRNA expression of placenta,fetal liver,newborn liver and liver of4weeksdramatically declined in IUGR group compared with untreated group.The mRNA andprotein expression of PI3K,AKT2and PGC-1a was obviously lower in placenta, fetal liverand newborn liver tissues of IUGR than untreated SD rats(P<0.05).The results above alsoapply to CG-IUGR and control groups of8weeks,however, the mRNA expression of IGF-2was not detected in both groups.TG level in plasma of IUGR group was obviously higherthan untreated groups, and mild fatty degeneration was only observed in hepatocytes ofIUGR group via Oil red staining, however, there was no difference in HE staining.Conclusions Decreases in transcriptional levels of IGF-2of CG-IUGR rats might causemetabolic syndrome by down-regulating PGC-1a,and PGC-1a might be a downstreammolecule of PI3K/AKT2pathway.