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

IF 2.9 4区生物学 Q3 CELL BIOLOGY

Journal of Molecular Histology Pub Date : 2025-03-29 DOI:10.1007/s10735-025-10398-3

Fanglei Yang, Yifan Mao, Bin Tang, Rui Xu, Feiyun Jiang

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引用次数: 0

Abstract

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.

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脂肪酸结合蛋白4敲低通过调节PTEN/Akt/mTOR信号通路介导的自噬改善妊娠期糖尿病大鼠胎儿发育

本研究旨在探讨脂肪酸结合蛋白4 （FABP4）敲低是否通过调节10号染色体上缺失的磷酸酶和紧张素同源物(PTEN)/丝氨酸/苏氨酸蛋白激酶B (Akt)/哺乳动物雷帕霉素靶蛋白（mTOR）信号通路介导的自噬来改善妊娠糖尿病（GDM）大鼠的胎儿发育。随机分配妊娠大鼠，设空白组（n = 12）、GDM组（n = 12）、小干扰阴性对照（si-NC）组（n = 12）、si-FABP4组（n = 12）、si-FABP4 + PTEN组（n = 12）。与空白组怀孕的老鼠相比,血清FABP4水平,堕胎率、空腹胰岛素、稳态模型评估胰岛素抵抗指数、发展畸形率和发生率胎儿宫内生长受限的老鼠,以及PTEN和Beclin-1蛋白质表达和轻链3 II型(LC3 -ΙI) / LC3 -Ι比率在胎盘组织中显著上升,而磷酸化(p)一种蛋白激酶/ Akt比率,p62蛋白表达,GDM + si-NC组胎盘组织P -mTOR/mTOR比值显著降低（P < 0.05）。FABP4敲低可改善GDM大鼠胎儿发育，其作用机制可能与通过调节PTEN/Akt/mTOR信号通路抑制自噬有关。

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来源期刊

Journal of Molecular Histology 生物-细胞生物学

CiteScore

5.90

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.