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,wh...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.PPARKIN/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.展开更多
文摘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.PPARKIN/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.
