On the other hand, increased intracellular UA is produced by xanthine oxidoreductase (XOR) or by uptake via urate transporters, thereby activating mitogen-activated protein kinases (MAPK) and NADPH oxidase, resulting in increased mitochondrial and cytoplasmic oxidative stress, which may be implicated in metabolic diseases [59]. This evidence concerns the gene FMO5 and metabolic disease.