College of Osteopathic Medicine, Touro University California, Vallejo.
Children's Hospital Oakland Research Institute, Oakland.
Curr Opin Clin Nutr Metab Care. 2018 Jul;21(4):277-282. doi: 10.1097/MCO.0000000000000469.
To review recent evidence for the role of dietary carbohydrate in de novo lipogenesis (DNL) and nonalcoholic fatty liver disease (NAFLD).
A large body of evidence suggests that increased hepatic DNL is a significant pathway contributing to the development of NAFLD. Dietary carbohydrates, in particular, fructose, have been shown to stimulate DNL and increase liver fat, although it is debated whether this is due to excess energy or fructose per se. Recent dietary intervention studies conducted in energy balance show that high-fructose diets increase DNL and liver fat, whereas fructose restriction decreases DNL and liver fat.
The association of high-carbohydrate and high-sugar diets with NAFLD may in part be explained by the effect of sugar on increasing hepatic DNL.
探讨膳食碳水化合物在肝脏从头合成脂肪（DNL）和非酒精性脂肪性肝病（NAFLD）中的作用的最新证据。
大量证据表明，肝内 DNL 的增加是导致 NAFLD 发展的重要途径。膳食碳水化合物，特别是果糖，已被证明可刺激 DNL 并增加肝脏脂肪，尽管尚不清楚这是由于能量过剩还是果糖本身所致。在能量平衡状态下进行的最近的饮食干预研究表明，高果糖饮食可增加 DNL 和肝脏脂肪，而果糖限制则可减少 DNL 和肝脏脂肪。
高碳水化合物和高糖饮食与 NAFLD 的关联部分可能是由于糖增加肝内 DNL 的作用所致。
