Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome; its rising prevalence parallels the rise in obesity and diabetes. Historically thought to result from overnutrition and a sedentary lifestyle, recent evidence suggests that diets high in sugar (from sucrose and/or high-fructose corn syrup [HFCS]) not only increase the risk of NAFLD, but also non-alcoholic steatohepatitis (NASH). Herein, we review the experimental and clinical evidence that fructose precipitates fat accumulation in the liver, due to both increased lipogenesis and impaired fat oxidation. Recent evidence suggests that the predisposition to fatty liver is linked to the metabolism of fructose by fructokinase C, which results in ATP consumption, nucleotide turnover and uric acid generation that mediate fat accumulation. Alterations to gut permeability, the microbiome, and associated endotoxemia contribute to the risk of NAFLD and NASH. Early clinical studies suggest that reducing sugary beverages and total fructose intake, especially from added sugars, may have a significant benefit on reducing hepatic fat accumulation. We suggest larger, more definitive trials to determine if lowering sugar/HFCS intake, and/or blocking uric acid generation, may help reduce NAFLD and its downstream complications of cirrhosis and chronic liver disease.

中文翻译：

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果糖和糖：非酒精性脂肪肝的主要调节因子

非酒精性脂肪肝（NAFLD）是代谢综合征的肝脏表现；其患病率的上升与肥胖症和糖尿病的上升并行。历史上认为是营养过剩和久坐不动的生活方式造成的，最近的证据表明，高糖饮食（来自蔗糖和/或高果糖玉米糖浆 [HFCS]）不仅会增加 NAFLD 的风险，还会增加非酒精性脂肪性肝炎 (NASH) ）。在此，我们回顾了实验和临床证据，即由于脂肪生成增加和脂肪氧化受损，果糖会导致肝脏中的脂肪堆积。最近的证据表明，脂肪肝的易感性与果糖激酶 C 对果糖的代谢有关，这会导致 ATP 消耗、核苷酸转换和尿酸生成，从而介导脂肪积累。肠道通透性、微生物组和相关内毒素血症的改变会增加 NAFLD 和 NASH 的风险。早期的临床研究表明，减少含糖饮料和总果糖的摄入量，尤其是添加糖的摄入量，可能对减少肝脏脂肪堆积有显着益处。我们建议进行更大规模、更明确的试验，以确定降低糖/HFCS 摄入量和/或阻止尿酸生成是否有助于减少 NAFLD 及其下游肝硬化和慢性肝病并发症。