It has been demonstrated as a significant adverse factor contributing to compromised outcomes such as IUGR/LBW and organ malformation.[41, 59, 64, 65, 66] Building upon our previously established PCE‐induced IUGR rat model,[38, 40, 41] this study focused on investigating the age‐related changes in glucose metabolism and insulin sensitivity, as well as elucidating the underlying programming mechanism. Here, INS is linked to fetal growth restriction.