Influence of Transcription Factor KLF16 on Lipid Metabolism in Non-alcoholic Fatty Liver Disease
10.13471/j.cnki.j.sun.yat-sen.univ（med.sci）.2024.0410
- VernacularTitle:转录因子KLF16对非酒精性脂肪肝病脂质代谢的影响
- Author:
Guanjun CAI
1
;
Xinyuan CUI
1
;
Wenyi LI
2
;
Wenfang PENG
1
Author Information
1. Department of Endocrinology， Tongren Hospital， Shanghai Jiao Tong University School of Medicine， Shanghai 200000， China
2. Shanghai Jiaotong University School of Medicine Hongqiao International Medical Research Institute， Shanghai 200000， China
- Publication Type:Journal Article
- Keywords:
Krüppel-like factor 16;
endoplasmic reticulum stress;
nonalcoholic fatty liver disease;
lipid metabolism;
adeno-associated virus;
gene knockdown
- From:
Journal of Sun Yat-sen University(Medical Sciences)
2024;45(4):582-592
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the expression of transcription factor KLF16 in nonalcoholic fatty liver disease （NAFLD） and its effect on lipid metabolism. MethodsAn animal model of NAFLD was constructed in mice induced by a high-fat diet. The mice were divided into normal diet group （ND） and high fat diet group （HFD）. NAFLD cell model was constructed by primary mouse liver cells induced by oleic acid. The cells were divided into control group （Control group） and oleic acid induction group （OA group）. Real-time fluorescence quantitative PCR （RT-qPCR） and Western blot were used to detect KLF16 expression in NAFLD animal and cell models. In vitro and in vivo models of KLF16 knockdown were constructed by injection of adeno-associated virus （AAV） into mouse tail veins and transient transfection of cell siRNA. Hematoxylin-eosin staining （HE） and other methods were used to detect changes in lipid deposition in NAFLD models before and after KLF16 knockout. RT-qPCR was used to detect the expression of key genes of lipid metabolism in both cellular and animal NAFLD models before and after KLF16 knockdown. Western blot assay was used to detect the expression of endoplasmic reticulum stress protein in NAFLD model before and after KLF16 knockdown. ResultsThe expression level of KLF16 was up-regulated in HFD group and OA group， and lipid deposition was increased in OA group after KLF16 was depressed. There was no change in TC level in hepatocytes between groups （P>0.05）， and TG level was increased in different degrees （P<0.05， P<0.001）. At the same time， the change of KLF16 expression also caused the change of ER stress protein expression in OA group. ConclusionThe transcription factor KLF16 may alleviate lipid deposition in nonalcoholic fatty liver disease by endoplasmic reticulum stress.
