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By knocking out the Uox gene, these mice completely lose the ability to degrade uric acid, resulting in a significant spike in serum uric acid levels and the spontaneous formation of hyperuricemia and urate nephropathy phenotypes [6-7]

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These compounds include pyruvate, which can be converted into acetyl-CoA and enter the tricarboxylic acid (TCA) cycle or be used for fatty acid synthesis, and -ketoglutarate, a precursor of glutamate and an intermediate of the TCA cycle