Nutrition and Obesity Group, Department of Nutrition and Food Science, University of the Basque Country (UPV/EHU) and Lucio Lascaray Research Institute, Vitoria, Spain.
Food Funct. 2018 Aug 15;9(8):4207-4215. doi: 10.1039/c8fo00930a.
Autophagy eliminates damaged cellular components. In the liver, it has been proposed that it mediates the breakdown of lipid droplets. This study aimed to compare the involvement of autophagy and the oxidative status in the effects of resveratrol and energy restriction as therapeutic tools for managing liver steatosis. In addition, potential additive or synergic effects were studied. Rats were fed a high-fat high-sucrose diet for 6 weeks and then divided into four experimental groups and fed a standard diet: a control group (C), a resveratrol-treated group (RSV, 30 mg kg-1 d-1), an energy restricted group (R, -15%), and an energy restricted group treated with resveratrol (RR). Liver triacylglycerols (TGs) were measured by Folch's method. TBARS, GSH, GSSG, GPx and SOD were assessed using commercial kits. The protein expression of beclin, atg5 and p62, as well as ratios of pSer555 ULK1/total ULK1, pSer757 ULK1/total ULK1 and LC3 II/I were determined by western blotting. Energy restriction increased the protein expression of beclin, atg5 and pSer757 ULK1/total ULK1 and LC3 II/I ratios, and reduced the protein expression of p62, thus indicating that it induced autophagy activation. The effects of resveratrol were similar but less marked than the hypocaloric diet. No differences were observed in oxidative stress determinants except for TBARS, which was decreased by energy restriction. In conclusion, resveratrol can reverse partially dietary-induced hepatic lipid accumulation, although less efficiently than energy restriction. The delipidating effect of energy restriction is mediated in part by the activation of autophagy; however, the involvement of this process in the effects of resveratrol is less clear.
自噬消除受损的细胞成分。在肝脏中，有人提出它介导脂滴的分解。本研究旨在比较自噬和氧化状态在白藜芦醇和能量限制作为治疗肝脂肪变性的工具中的作用。此外，还研究了潜在的附加或协同作用。大鼠喂食高脂肪高蔗糖饮食 6 周，然后分为四个实验组并喂食标准饮食：对照组（C）、白藜芦醇处理组（RSV，30mgkg-1d-1）、能量限制组（R，-15%）和能量限制联合白藜芦醇处理组（RR）。采用 Folch 法测定肝三酰甘油（TGs）。采用商业试剂盒测定 TBARS、GSH、GSSG、GPx 和 SOD。通过 Western blot 测定 beclin、atg5 和 p62 的蛋白表达，以及 pSer555ULK1/总 ULK1、pSer757ULK1/总 ULK1 和 LC3 II/I 的比值。能量限制增加了 beclin、atg5 和 pSer757ULK1/总 ULK1 的蛋白表达和 LC3 II/I 的比值，并降低了 p62 的蛋白表达，表明其诱导了自噬的激活。白藜芦醇的作用与低热量饮食相似，但不如低热量饮食明显。除 TBARS 外，氧化应激标志物无差异，能量限制可降低 TBARS。总之，白藜芦醇可以部分逆转饮食诱导的肝脂质堆积，但效率低于能量限制。能量限制的去脂作用部分通过自噬的激活介导；然而，自噬在白藜芦醇作用中的参与尚不清楚。
