Non-alcoholic fatty liver disease is associated with ageing, and impaired mitochondrial homeostasis is the main cause for hepatic ageing. Caloric restriction (CR) is a promising therapeutic approach to reduce fatty liver. The present study aimed to investigate the effect of early onset CR on decelerating the progression of ageing-related steatohepatitis. The potential mechanisms regarding to mitochondria were further evaluated. Eight-week-old C57BL/6 male mice (n = 21) were randomly divided into three groups, Young-AL (AL, ad libitum), Aged-AL, and Aged-CR (60% intake of AL). Mice were sacri ced at the age of 7 months (Young) or 20 months (Aged). Aged-AL mice displayed the greatest body weight, liver weight and liver relative weight among treatments. Ageing caused a great grade of steatosis, lipid peroxidation, in ammation, and brosis in the liver. Mega mitochondria with short, randomly organized crista were noticed in the aged liver. CR ameliorated these negative phenomena in aged liver. Ageing was accompanied with a lower level of hepatic ATP, while CR restored it. Mitochondrial-related protein expressions of respiratory chain complexes (NDUFB8 and SDHB), and ssion (DRP1) were suppressed in aged liver. Proteins related to mitochondrial biogenesis (TFAM), and fusion (MFN2) were upregulated in aged liver. CR reversed the expressions of SDHB, TFAM, DRP1, and MFN2 in aged liver. To conclude, early onset CR signi cantly prevented the negative effect of ageing-associated steatohepatitis, including lipid peroxidation, in ammation, steatosis and brosis. Moreover, CR eased ageing-associated energy de cit in liver partially via maintaining mitochondrial homeostasis.
Non-alcoholic fatty liver disease is associated with ageing, and impaired mitochondrial homeostasis is the main cause for hepatic ageing. Caloric restriction (CR) is a promising therapeutic approach to reduce fatty liver. The present study aimed to investigate the effect of early onset CR on decelerating the progression of ageing-related steatohepatitis. The potential mechanisms regarding to mitochondria were further evaluated. Eight-week-old C57BL/6 male mice (n = 21) were randomly divided into three groups, Young-AL (AL, ad libitum), Aged-AL, and Aged-CR (60% intake of AL). Mice were sacrificed at the age of 7 months (Young) or 20 months (Aged). Aged-AL mice displayed the greatest body weight, liver weight and liver relative weight among treatments. Ageing caused a great grade of steatosis, lipid peroxidation, inflammation, and fibrosis in the liver. Mega mitochondria with short, randomly organized crista were noticed in the aged liver. CR ameliorated these negative phenomena in aged liver. Ageing was accompanied with a lower level of hepatic ATP, while CR restored it. Mitochondrial-related protein expressions of respiratory chain complexes (NDUFB8 and SDHB), and fission (DRP1) were suppressed in aged liver. Proteins related to mitochondrial biogenesis (TFAM), and fusion (MFN2) were upregulated in aged liver. CR reversed the expressions of SDHB, TFAM, DRP1, and MFN2 in aged liver. To conclude, early onset CR significantly prevented the negative effect of ageing-associated steatohepatitis, including lipid peroxidation, inflammation, steatosis and fibrosis. Moreover, CR eased ageing-associated energy deficit in liver partially via maintaining mitochondrial homeostasis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.