Graduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 100, Taiwan.
Department of Pediatrics, College of Medicine and Hospital, National Taiwan University, Taipei 100, Taiwan.
Mar Drugs. 2019 Jun 25;17(6):380. doi: 10.3390/md17060380.
Obesity is known to cause skeletal muscle wasting. This study investigated the effect and the possible mechanism of fish oil on skeletal muscle wasting in an obese rat model. High-fat (HF) diets were applied to induce the defects of lipid metabolism in male Sprague-Dawley rats with or without substitution of omega-3 fatty acids-enriched fish oil (FO, 5%) for eight weeks. Diets supplemented with 5% FO showed a significant decrease in the final body weight compared to HF diet-fed rats. The decreased soleus muscle weights in HF diet-fed rats could be improved by FO substitution. The decreased myosin heavy chain (a muscle thick filament protein) and increased FOXO3A and Atrogin-1 (muscle atrophy-related proteins) protein expressions in soleus muscles of HF diet-fed rats could also be reversed by FO substitution. FO substitution could also significantly activate adenosine monophosphate (AMP)-activated protein kinase (AMPK) phosphorylation, peroxisome-proliferator-activated receptor-γ (PPARγ) coactivator 1α (PGC-1α), and PPARγ protein expression and lipoprotein lipase (LPL) mRNA expression in soleus muscles of HF diet-fed rats. These results suggest that substitution of FO exerts a beneficial improvement in the imbalance of lipid and muscle metabolisms in obesity. AMPK/PGC-1α signaling may play an important role in FO-prevented obesity-induced muscle wasting.
肥胖已知可导致骨骼肌消耗。本研究探讨了鱼油对肥胖大鼠模型中骨骼肌消耗的影响及其可能的机制。高脂肪（HF）饮食用于诱导雄性 Sprague-Dawley 大鼠的脂代谢缺陷，或用富含ω-3 脂肪酸的鱼油（FO，5%）替代 HF 饮食 8 周。与 HF 饮食喂养的大鼠相比，补充 5%FO 的饮食显示出显著降低的最终体重。HF 饮食喂养的大鼠比目鱼肌重量的减少可以通过 FO 替代来改善。FO 替代还可以逆转 HF 饮食喂养的大鼠比目鱼肌中肌球蛋白重链（肌肉粗丝蛋白）的减少和 FOXO3A 和 Atrogin-1（肌肉萎缩相关蛋白）的增加。FO 替代还可以显著激活 AMP 激活的蛋白激酶（AMPK）磷酸化、过氧化物酶体增殖物激活受体-γ（PPARγ）共激活因子 1α（PGC-1α）和 PPARγ 蛋白表达以及脂蛋白脂肪酶（LPL）mRNA 表达在 HF 饮食喂养的大鼠比目鱼肌中。这些结果表明，FO 的替代对肥胖中脂质和肌肉代谢的失衡具有有益的改善作用。AMPK/PGC-1α 信号通路可能在 FO 预防肥胖引起的肌肉消耗中发挥重要作用。
