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Notably, the deletion of lipogenic enzymes in the liver, such as acetyl-CoA carboxylase 1/2 (ACC1/2), has been reported to liberate NADPH for antioxidant processes, including GSH regeneration 87

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Moreover, interplay between these processes and oxidative metabolism, which may contribute to hepatic cell damage, has been suggested to occur in the steatotic liver [28,29]

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A pilot study by Jackson et al