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Additionally, accelerated ATP degradation under pathological conditions (e.g., intense exercise and ischemiareperfusion injury) promotes hypoxanthine accumulation, creating a secondary drive for UA overproduction (Uskudar Cansu et al., 2019)

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Finally, the gut microbiome may contribute to NAFLD pathogenesis: an increased intestinal permeability could lead to the entry of endotoxins in portal circulation and activation, through toll-like receptor 4, of Kupffer cells, with consequent inflammation (5053)