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Several mechanisms including glucotoxicity, lipotoxicity, altered secretion of adipokines/cytokines, hepatokines (mainly higher circulating fetuin-A levels), stimulation of multiple inflammatory pathways, reduced bile-acid synthesis, endoplasmic reticulum stress, increased oxidative stress, mitochondrial dysfunction and alterations in gut microbiota/gut-derived endotoxins, in a complex interplay with genetic predisposition, drive the evolution of inflammation, hepatocellular injury and fibrosis [24–26]

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