Depletion of ApoA5 aggravates spontaneous and diet-induced nonalcoholic fatty liver disease by reducing hepatic NR1D1 in hamsters
Jiabao Guo, Guolin Miao, Wenxi Zhang, Haozhe Shi, Pingping Lai, Yitong Xu, Lianxin Zhang, Gonglie Chen, Yufei Han, Ying Zhao, G. Liu, Ling Zhang, Yuhui Wang, Wei Huang, Xunde Xian
Abstract
Our data demonstrate that HTG caused by ApoA5 deficiency in hamsters is sufficient to elicit hepatic steatosis and HFD aggravates NAFLD by reducing hepatic NR1D1 mRNA and protein levels, which provides a mechanistic link between ApoA5 and NAFLD and suggests the new insights into the potential therapeutic approaches for the treatment of HTG and the related disorders due to ApoA5 deficiency in the clinical trials in future.
Topics & Concepts
LipolysisEndocrinologyInternal medicineSteatosisFatty liverAdipose tissueLipoprotein lipaseNonalcoholic fatty liver diseaseHamsterSteatohepatitisTriglycerideHepatic lipaseBiologyHypertriglyceridemiaMedicineCholesterolDiseaseAdipose Tissue and MetabolismLiver Disease Diagnosis and TreatmentLipid metabolism and disorders