Mechanistic on the Regulation of Insulin Resistance in HepG2 Cells by SLC39A14
10.11969/j.issn.1673-548X.2025.08.018
- VernacularTitle:SLC39A14调控HepG2细胞胰岛素抵抗的机制研究
- Author:
Huiping LI
1
;
Yingfang LI
1
;
Jihua HUANG
1
Author Information
1. 530007 南宁,广西医科大学第二附属医院内分泌科
- Publication Type:Journal Article
- Keywords:
Iron overload;
Insulin resistance;
SLC39A14;
Fer-1;
Ferroptosis
- From:
Journal of Medical Research
2025;54(8):108-113,128
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect and mechanism of solute carrier family 39 member 14(SLC39A14)on iron overload-induced insulin resistance in HepG2 cells.Methods HepG2 cells were cultured in vitro,and different concentrations of ferric ammonium citrate(FAC)were added to detect cell viability by CCK-8,calcein-AM was used to detect unstable iron pools(LIP),mi-tochondria were observed by transmission electron microscopy,and insulin resistance was detected by cellular glucose consumption,as well as the expression of SLC39A14 protein and mRNA.Subsequently,Ferrostatin-1(Fer-1)was added to detect reactive oxygen spe-cies(ROS),malondialdehyde(MDA)and glutathione(GSH).Finally,small interfering RNA(siRNA)technology was used to knock down the expression of SLC39A14 to observe whether oxidative stress and insulin resistance indices changed.Results After FAC inter-vention,cell viability decreased,the LIP level increased,and glucose consumption reduced.Additionally,the protein and mRNA expres-sion of SLC39A14 was upregulated.Compared with the FAC group,the co-treatment of FAC and Ferrostatin-1 ameliorated the intracel-lular oxidative stress by decreasing the levels of ROS and MDA and increasing the levels of GSH,down-regulating the protein and mRNA expression of SLC39A14,and increasing the glucose consumption,thereby alleviating the onset of insulin resistance.After knockdown of SLC39A14,the levels of oxidative stress and insulin resistance in HepG2 cells in the FAC+SLC39A14 knockdown group were further im-proved compared with those in the FAC group.Conclusion FAC intervention caused the development of insulin resistance in HepG2 cells by a mechanism that may be related to activation of SLC39A14.
