Fatty acid binding protein 4 knockdown improves fetal development in rats with gestational diabetes mellitus through modulating autophagy mediated by the PTEN/Akt/mTOR signaling pathway.

We aimed to investigate whether fatty acid binding protein 4 (FABP4) knockdown can ameliorate fetal development in rats with gestational diabetes mellitus (GDM) through modulating autophagy mediated by the phosphatase and tensin homolog deleted on chromosome ten (PTEN)/serine/threonine protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway. Blank group (n = 12), GDM group (n = 12), small interfering negative control (si-NC) group (n = 12), si-FABP4 group (n = 12), and si-FABP4 + PTEN group (n = 12) were set up for the random assignment of pregnant rats. Compared to the blank group of pregnant rats, the serum FABP4 level, abortion rate, fasting insulin, homeostasis model assessment of insulin resistance index, development malformation rate and incidence rate of intrauterine growth restriction of fetal rats, as well as PTEN and Beclin-1 protein expressions and light chain 3 type II (LC3-ΙI)/LC3-Ι ratio in placental tissues rose significantly, while the phosphorylated (p)-Akt/Akt ratio, p62 protein expression, and p-mTOR/mTOR ratio in placental tissues dropped significantly in the GDM plus si-NC group (P < 0.05). FABP4 knockdown improves fetal development in GDM rats, and its mechanism of action is probably related with the inhibited autophagy by regulating the PTEN/Akt/mTOR signaling pathway.