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

{"title":"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","authors":"Fanglei Yang, Yifan Mao, Bin Tang, Rui Xu, Feiyun Jiang","doi":"10.1007/s10735-025-10398-3","DOIUrl":null,"url":null,"abstract":"<div>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.</div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Molecular Histology","FirstCategoryId":"99","ListUrlMain":"https://link.springer.com/article/10.1007/s10735-025-10398-3","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

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.

Abstract Image

查看原文本刊更多论文

求助全文

约1分钟内获得全文求助全文

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.