Department of Bioengineering and Environmental Science, Changsha University, Changsha 410003, Hunan, PR China; Collaborative Innovation Center for Efficient and Health Production of Fisheries in Hunan Province, Changde 415000, Hunan, PR China.
Department of Bioengineering and Environmental Science, Changsha University, Changsha 410003, Hunan, PR China; Hunan Provincial Key Laboratory of Nutrition and Quality Control of Aquatic Animals, Department of Biological and Environmental Engineering, Changsha University, Changsha 410022, PR China.
Comp Biochem Physiol B Biochem Mol Biol. 2020 Feb;240:110331. doi: 10.1016/j.cbpb.2019.110331. Epub 2019 Aug 25.
The present study was performed to determine the effect of high fat diet in lipid accumulation, oxidative stress and autophagy, and to explore the underlying molecular mechanism of high fat diet induced hepatic oxidative damage in Chinese softshell turtle. To this end, the control group were fed a normal fat diet (NFD, 6.38% lipid) and the experimental group were bred high fat diet (HFD, 13.89% lipid) for eight weeks. Lipid accumulation, oxidative stress and autophagy, as well as the mRNA expression of genes related to the antioxidant system were determined in the liver. Results showed that high fat diet not only exacerbated lipid accumulation in the liver and serum through increasing contents of triglyceride, total cholesterol and low-density lipoprotein and decreasing content of high-density lipoprotein, but also induced liver injury through increasing activities of alanine aminotransferase and aspartate aminotransferase in the serum. In addition, the experimental subject induced oxidative injury for the increase of reactive oxygen species, malondialdehyde and protein carbonyl contents and the reduction of glutathione contents, anti-superoxide anion capacity and catalase, total superoxide dismutase, glutathione peroxidase, glutathione-S transferase activities. Meanwhile, antioxidant-related signaling molecule expression were also decreased, which might attribute to regulate antioxidant-related signaling molecule. On top of that, it indicated promote the occurrence of liver autophagy via up-regulating expressions of AMP activated protein kinase, UNC-51-like kinase 1, Microtubule-associated proteins 1A/1B light chain 3 and down-regulating gene expression of mammalian target of rapamycin. In conclusion, high fat diet could enhance lipid accumulation in the liver and serum, lead to liver injury and oxidative damage, impair liver antioxidant capacity, regulate antioxidant-related signaling molecule expression and activate hepatic autophagy.
本研究旨在确定高脂肪饮食对脂质积累、氧化应激和自噬的影响，并探讨中华鳖肝脏氧化损伤的潜在分子机制。为此，对照组投喂正常脂肪饮食（NFD，6.38%脂肪），实验组投喂高脂肪饮食（HFD，13.89%脂肪），为期 8 周。检测了肝脏中的脂质积累、氧化应激和自噬，以及与抗氧化系统相关的基因的 mRNA 表达。结果表明，高脂肪饮食不仅通过增加甘油三酯、总胆固醇和低密度脂蛋白的含量，降低高密度脂蛋白的含量，加剧了肝脏和血清中的脂质积累，还通过增加血清中丙氨酸氨基转移酶和天冬氨酸氨基转移酶的活性导致肝损伤。此外，实验动物通过增加活性氧、丙二醛和蛋白质羰基的含量以及降低谷胱甘肽的含量、超氧化物阴离子清除能力和过氧化氢酶、总超氧化物歧化酶、谷胱甘肽过氧化物酶、谷胱甘肽-S-转移酶的活性，诱导氧化损伤。同时，抗氧化相关信号分子的表达也降低，这可能归因于调节抗氧化相关信号分子。此外，通过上调 AMP 激活蛋白激酶、UNC-51 样激酶 1、微管相关蛋白 1A/1B 轻链 3 的表达和下调哺乳动物雷帕霉素靶蛋白的基因表达，表明促进肝脏自噬的发生。总之，高脂肪饮食可增强肝脏和血清中的脂质积累，导致肝损伤和氧化损伤，损害肝脏抗氧化能力，调节抗氧化相关信号分子的表达，激活肝脏自噬。
