Non-alcoholic fatty liver disease (NAFLD) has recently become a public health concern concurrent with the obesity crisis. Previous work has shown aberrant mitochondrial content/quality and autophagy in models of NAFLD, whereas exercise is known to improve these derangements. The purpose of this study was to examine the effect of different weight-loss modalities on hepatic mitochondrial content, autophagy and mitophagy in NAFLD. Forty-eight male C57BL/6J mice were divided into 1 of 4 groups: low fat diet (LFD, 10% fat, 18 weeks), high fat diet (HFD, 60% fat diet, 18 weeks), weight-loss by diet (D, 60% fat diet for 10 weeks then 10% fat diet for 8 weeks) or weight-loss by diet and physical activity (D/PA, 60% fat diet for 10 weeks, then 10% fat diet plus a running wheel for 8 weeks). Immunoblot data were analyzed by one-way analysis of variance (ANOVA) with significance denoted at p < 0.05. COX-IV protein contents were approximately 50% less in HFD compared to LFD. D/PA had 50% more BNIP3 compared to HFD. PINK1 content was 40% higher in D and D/PA compared to LFD. P-PARKIN/PARKIN levels were 40% lower in HFD, D, and D/PA compared to LFD. Whereas p-UbSer65 was 3-fold higher in HFD. LC3II/I ratio was 50% greater in HFD and D/PA, yet p62 protein content was 2.5 fold higher in HFD. High-fat diet causes disruptions in markers of mitochondrial quality control. Physical activity combined with diet were able to ameliorate these derangements and seemingly improve hepatic mitochondrial quality above control values.
Keywords: Autophagy; Hepatic metabolism; High-fat diet; Mitochondria.
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