At the same time, they also established a PCE-induced intrauterine growth retardation (IUGR) model in rats to elucidate the role of altered glucose transport function mediated by altered GC- insulin-like growth factor-1 (IGF1)-GLUT1 axis programming in the development of fetal-originated OA and its epigenetic mechanism, providing a theoretical basis for the early prevention and treatment of OA. This evidence concerns the gene SLC2A1 and fetal growth restriction.