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In contrast, under high-SUAassociated stress conditions, available evidence suggests that AMPK signaling may be suppressed or functionally insufficient, shifting ACC-mediated regulation toward a more lipogenic state and contributing to hepatic lipid accumulation.Concurrently, impaired autophagic flux,particularly dysregulated lipophagy,may reduce the efficiency of lipid droplet degradation and clearance, thereby further exacerbating intracellular lipid overload