The development of mammalian nonalcoholic fatty liver disease is associated with oxidative stress, reduced mitochondrial function, and increased apoptosis in hepatocytes; however, the expressions of mitochondria-related genes are elevated in goose fatty liver, suggesting that there may be a unique protective mechanism in goose fatty liver. The aim of the study was to investigate this protective mechanism in terms of anti-oxidant capacity. Our data showed no substantial differences in the mRNA expression levels of the apoptosis-related genes including B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax), cysteinyl aspartate-specific proteinase-3 (Caspase-3), and cysteinyl aspartate-specific proteinase-9 (Caspase-9) in the livers of the control and overfeeding Lander geese groups. The protein expression levels of Caspase-3 and cleaved Caspase-9 were not markedly different between the groups. Compared with the control group, malondialdehyde content was significantly lower (P < 0.01), glutathione peroxidase (GSH-Px) activity, glutathione (GSH) content, and mitochondrial membrane potential levels were higher (P < 0.01) in the overfeeding group. The mRNA expression levels of the anti-oxidant genes superoxide dismutase 1 (SOD1), glutathione peroxidase 1 (GPX1), and glutathione peroxidase 2 (GPX2) were increased in goose primary hepatocytes after 40 mM and 60 mM glucose treatment. Reactive oxygen species (ROS) levels were significantly reduced (P < 0.01), whereas the mitochondrial membrane potential was maintained at normal levels. The mRNA expression levels of the apoptosis-related genes Bcl-2, Bax, and Caspase-3 were not substantial. There were no significant differences in the expression levels of Caspase-3 and cleaved Caspase-9 proteins. In conclusion, glucose-induced enhanced anti-oxidant capacity may help protect the function of mitochondria and inhibit the occurrence of apoptosis in goose fatty liver.
Keywords: anti-oxidant; apoptosis; fatty liver; goose; mitochondria.
No significant pathological symptoms were observed in the liver of goose after overfeeding, suggesting that a specific protection mechanism exists in goose liver. Previous studies have shown that mitochondria may participate in the formation of goose fatty liver by improving its energy metabolism and the production of precursor metabolites. To further understand the role of mitochondria in the formation of goose fatty liver, the present study investigated the changes of mitochondrial function, anti-oxidant capacity, and apoptosis in goose fatty liver. There were found that the level of mitochondrial membrane potential was increased, no apoptosis was observed and anti-oxidant capacity was improved in goose fatty liver, no apoptosis was observed and anti-oxidant genes expressions were increased in goose primary hepatocytes after 40 mM glucose treatment. Our findings imply that apoptosis is inhibited by glucose-induced enhanced anti-oxidant activity in goose fatty liver. Our study not only contributes to revealing the protective mechanism in goose fatty liver but also providing new references for the study of nonalcoholic fatty liver in mammals.
© The Author(s) 2023. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.