I Clinica Medica, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, 00161 Rome, Italy.
Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00161 Rome, Italy.
Nutrients. 2022 Mar 8;14(6):1127. doi: 10.3390/nu14061127.
Non-alcoholic fatty liver disease (NAFLD) represents the most common chronic liver disease and it is considered the hepatic manifestation of metabolic syndrome (MetS). Diet represents the key element in NAFLD and MetS treatment, but some nutrients could play a role in their pathophysiology. Among these, fructose added to foods via high fructose corn syrup (HFCS) and sucrose might participate in NAFLD and MetS onset and progression. Fructose induces de novo lipogenesis (DNL), endoplasmic reticulum stress and liver inflammation, promoting insulin resistance and dyslipidemia. Fructose also reduces fatty acids oxidation through the overproduction of malonyl CoA, favoring steatosis. Furthermore, recent studies suggest changes in intestinal permeability associated with fructose consumption that contribute to the risk of NAFLD and MetS. Finally, alterations in the hunger-satiety mechanism and in the synthesis of uric acid link the fructose intake to weight gain and hypertension, respectively. However, further studies are needed to better evaluate the causal relationship between fructose and metabolic diseases and to develop new therapeutic and preventive strategies against NAFLD and MetS.
非酒精性脂肪性肝病 (NAFLD) 是最常见的慢性肝病，被认为是代谢综合征 (MetS) 的肝脏表现。饮食是 NAFLD 和 MetS 治疗的关键因素，但某些营养素可能在其发病机制中发挥作用。其中，通过高果糖玉米糖浆 (HFCS) 和蔗糖添加到食物中的果糖可能参与 NAFLD 和 MetS 的发生和进展。果糖诱导从头合成脂肪 (DNL)、内质网应激和肝脏炎症，促进胰岛素抵抗和血脂异常。果糖还通过过量生成丙二酰辅酶 A 减少脂肪酸氧化，有利于脂肪变性。此外，最近的研究表明，与果糖消耗相关的肠道通透性改变可能导致 NAFLD 和 MetS 的风险增加。最后，饥饿-饱腹感机制和尿酸合成的改变将果糖摄入与体重增加和高血压联系起来。然而，需要进一步的研究来更好地评估果糖与代谢性疾病之间的因果关系，并开发针对 NAFLD 和 MetS 的新治疗和预防策略。
