Laboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Comalcalco, Tabasco, Mexico.
Arch Physiol Biochem. 2023 Feb;129(1):233-240. doi: 10.1080/13813455.2020.1812666. Epub 2020 Sep 3.
Identification of new modifications and the association with diet patterns are essential for the prevention of non-alcoholic fatty liver disease (NAFLD). To address this problem, we feed rats with high caloric diets based on high sucrose (HSD) and high fat (HFD) and analysed metabolic and mitochondrial alterations. Both diets induce moderated obesity and fat accumulation in the liver after 8, 10 and 12 months of diet. The HSD induces both hyperleptinemia and hyperinsulinemia, as well as up-regulation of transcription factors SRBEP1 and PPARγ along slight increase nitrosylation of proteins and increased mitochondrial fission. In contrast, HFD induced hyperleptinemia without changes in neither insulin levels nor oxidative stress, SREBP1, PPARγ, or mitochondrial dynamics. In conclusion, chronic consumption of high sucrose content diets induces more pathological and metabolic alteration in liver in comparison with consumption of high-fat content diets, although both induces obesity and liver steatosis in these animal models.
鉴定新的修饰物并将其与饮食模式相关联对于预防非酒精性脂肪性肝病（NAFLD）至关重要。为了解决这个问题，我们用高蔗糖（HSD）和高脂肪（HFD）的高热量饮食喂养大鼠，并分析了代谢和线粒体的改变。两种饮食在 8、10 和 12 个月的饮食后都会导致适度的肥胖和肝脏脂肪堆积。HSD 会导致高瘦素血症和高胰岛素血症，以及转录因子 SRBEP1 和 PPARγ 的上调，同时轻度增加蛋白质的硝化和线粒体分裂。相比之下，HFD 诱导高瘦素血症，而胰岛素水平、氧化应激、SREBP1、PPARγ 或线粒体动力学均无变化。总之，与高脂肪含量饮食相比，慢性摄入高蔗糖含量饮食会在肝脏中引起更多的病理和代谢改变，尽管这两种饮食都会导致这些动物模型肥胖和肝脂肪变性。
