Exercise intervention improves mitochondrial quality in non-alcoholic fatty liver disease zebrafish

• DOI: 10.3389/fendo.2023.1162485
• Publication Date: 2023-05-22T04:44:12Z
• Authors: Yun-Yi Zou; Xiang-bin Tang; Zhang-Lin Chen; Bin Liu; Lan Zheng; Ming-Yang Song; Qin Xiao; Zuo-Qiong Zhou; Xi-Yang Peng; Chang-Fa Tang
• Keywords: MFN2; PINK1; Sequestosome 1; TFAM

Introduction Recent reports indicate that mitochondrial quality decreases during non-alcoholic fatty liver disease (NAFLD) progression, and targeting the mitochondria may be a possible treatment for NAFLD. Exercise can effectively slow NAFLD progression or treat However, effect of exercise on in has not yet been established. Methods In present study, we fed zebrafish high-fat diet to model NAFLD, subjected swimming exercise. Results After 12 weeks, significantly reduced diet-induced injury, inflammation fibrosis markers. Swimming improved morphology dynamics, inducing upregulation optic atrophy 1(OPA1), dynamin related protein 1 (DRP1), mitofusin 2 (MFN2) expression. also activated biogenesis via sirtuin (SIRT1)/ AMP-activated kinase (AMPK)/ PPARgamma coactivator alpha (PGC1α) pathway, mRNA expression genes acid oxidation oxidative phosphorylation. Furthermore, find mitophagy was suppressed with decreased numbers mitophagosomes, inhibition PTEN-induced (PINK1) – parkin RBR E3 ubiquitin ligase (PARKIN) pathway sequestosome (P62) Notably, partially recovered number which associated upregulated PARKIN p62 Discussion These results demonstrate could alleviate effects mitochondria, suggesting beneficial treating