Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, Italy; Department of Anatomical, Histological, Forensic Medicine and Orthopedic Sciences, Sapienza University of Rome, Italy.
Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, Italy.
Nutrition. 2020 Jul-Aug;75-76:110782. doi: 10.1016/j.nut.2020.110782. Epub 2020 Mar 5.
Non-alcoholic fatty liver disease (NAFLD) has become the most common liver disease globally. It is caused by a complex network of factors, including diet. The hallmark of NAFLD is the benign accumulation of triacylglycerols, however, this condition may worsen into non-alcoholic steatohepatitis (NASH), a more severe form associated with inflammation and fibrosis. Currently, no therapies are available, and diet modifications are the only strategy. Although there is increasing evidence emerging about how an abuse of carbohydrates could be involved in the progression of liver injury, a comprehensive understanding of the damage induced by an enriched carbohydrate diet is still far from complete. The aim of this study was to investigate and compare the effects of a low-fat/high-carbohydrate diet (LF-HCD) with high-fat (HFD) and standard (SD) diets in a nutritional mouse model of NAFLD/NASH.
Histologic, real-time polymerase chain reaction, and immunohistochemical evaluations were performed.
The results showed that the prolonged abuse of both LF-HCDs and HFDs induced a significant increase in hepatic steatosis, inflammation, and fibrosis scores compared with SD. At the same time, both LF-HCDs and HFDs led to significant increases in the expression of the molecules involved in the progression of NAFLD that we assessed (perilipin, CD68, TGF-β1, CTGF, leptin, leptin receptor, and α-SMA).
The present study highlighted that the simple substitution of fats with carbohydrates is not a proper strategy to prevent or mitigate the progression of NAFLD/NASH. Further studies are required to define the best nutritional strategy to prevent NAFLD and its related metabolic syndrome.
非酒精性脂肪性肝病（NAFLD）已成为全球最常见的肝脏疾病。它是由包括饮食在内的多种因素复杂网络引起的。NAFLD 的标志是三酰甘油的良性积累，然而，这种情况可能会恶化成非酒精性脂肪性肝炎（NASH），这是一种更严重的炎症和纤维化相关形式。目前，尚无治疗方法，饮食改变是唯一策略。尽管越来越多的证据表明，碳水化合物的滥用可能与肝损伤的进展有关，但对富含碳水化合物的饮食所引起的损伤的全面了解还远远不够。本研究旨在调查和比较低脂肪/高碳水化合物饮食（LF-HCD）与高脂肪（HFD）和标准（SD）饮食在 NAFLD/NASH 营养模型小鼠中的作用。
进行了组织学、实时聚合酶链反应和免疫组织化学评估。
结果表明，与 SD 相比，LF-HCD 和 HFD 的长期滥用均导致肝脂肪变性、炎症和纤维化评分显著增加。同时，LF-HCD 和 HFD 均导致我们评估的 NAFLD 进展相关分子（脂联素、CD68、TGF-β1、CTGF、瘦素、瘦素受体和α-SMA）的表达显著增加。
本研究强调，用碳水化合物简单替代脂肪不是预防或减轻 NAFLD/NASH 进展的适当策略。需要进一步研究以确定预防 NAFLD 及其相关代谢综合征的最佳营养策略。
