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. Author manuscript; available in PMC: 2019 Aug 1.
Published in final edited form as: Hepatology. 2018 May 21;68(2):496–514. doi: 10.1002/hep.29849

Fig. 7. Hepatocyte-specific deletion of SIRT1 disrupts DEPTOR signaling, stimulates mTORC1 activity, and exacerbates the development of alcoholic fatty liver and liver injury in mice.

Fig. 7

A. Protein levels of SIRT1 are measured in AML12 hepatocytes and in livers of wild-type (WT) mice and SIRT1 liver-specific knockout (SIRT1 LKO) mice under conditions of normal and ethanol exposure. B. Hepatocyte-specific deletion of SIRT1 downregulates DEPTOR and enhances mTORC1 activation in mice after chronic-binge ethanol feeding. C. Genetic ablation of SIRT1 in the liver increases the susceptibility to alcohol-induced fatty liver. D. Hepatic SIRT1 deficiency exacerbates alcohol-mediated abnormalities of lipid metabolism in mice. E–F. Hepatic SIRT1 loss aggravates alcohol-induced inflammation, apoptosis, and liver injury. The data are presented as the mean ± SEM, n = 4–8. *P < 0.05, vs. pair-fed WT mice; #P < 0.05, vs. ethanol-fed WT mice.