Plausibly, a bidirectional interaction exists between SUA and central obesity: on one hand, high fructose intake activates carbohydrate-responsive element-binding protein (ChREBP) and upregulates fatty acid synthase (FAS), promoting lipogenesis and fat deposition [60]; on the other hand, excess adipose tissue increases leptin secretion, which activates the renin–angiotensin–aldosterone system (RAAS) and impairs renal uric acid excretion [61]. The gene discussed is FAS; the disease is Abdominal obesity.