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Glycine -methyltransferase deletion in mice diverts carbon flux from gluconeogenesis to pathways that utilize excess methionine cycle intermediates

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The key is to get to that root cause, and not to just suppress symptoms with an acid blocker, which often makes things worse

200 Uric acid is implicated in the pathogenesis of metabolic syndrome through its ability to induce insulin resistance and promote low-grade inflammation, underscoring its proinflammatory role