Therefore, together with the evidences that “mitochondrial organization,” “mitochondrion morphogenesis,” and “mitochondrial inner membrane” terms were dysregulated in the proliferative endometrium of LRP sows and that uterine insulin resistance beginning before pregnancy induced mitochondrial dysfunction (evidenced by decreased Mfn2, Opa1, and Fis1) during the implantation window in mouse uteri from the HFD group, we concluded that mitochondrial dysfunction, but not the endoplasmic reticulum stress, underlaid uterine insulin resistance-induced impaired reproductive performance. This evidence concerns the gene OPA1 and Insulin resistance.