Coenzyme Q10 (CoQ10) is a well-known anti-adipogenic factor that possesses the capability to regulate non-alcoholic fatty liver disease (NAFLD). However, the mechanism by which CoQ10 acts on NAFLD is still unclear. In this study, the role of CoQ10 in the prevention of NAFLD was investigated in vivo and in vitro. C57BL/6J mice were fed a normal diet, high-fat diet (HFD) or HFD supplemented with CoQ10 (1800 mg kg⁻¹ HFD) for 24 weeks. HepG2 cells were treated with sodium palmitate for investigating the mechanism of action of CoQ10 on NAFLD. The results showed that CoQ10 alleviated HFD-induced weight gain and NAFLD, accompanied by an anti-hyperlipidaemia effect, by reducing the serum triglycerides, total cholesterol, and low-density lipoprotein cholesterol levels. Importantly, CoQ10 could downregulate the expression of sterol regulatory element-binding protein-1c (SREBP-1c), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS), which are related to lipid synthesis, and upregulate the expression of peroxisome proliferator-activated receptors α (PPARα) and carnitine palmitoyltransferase-1 (CPT-1) associated with fatty acid oxidation. Similar to the results from mice, treatment with CoQ10 alleviated sodium palmitate-induced hepatocyte steatosis via the inhibition of lipogenesis and promotion of fatty acid oxidation. However, Compound C, as an AMPK inhibitor, could significantly block the benefits derived from CoQ10 treatment. In conclusion, CoQ10 could serve as an AMPK activator and regulate the hepatic lipid metabolism to inhibit the abnormal accumulation of hepatic lipids and prevent NAFLD progression.

中文翻译：

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辅酶Q10通过激活AMPK途径来减轻高脂饮食诱导的非酒精性脂肪肝疾病†

辅酶Q10（CoQ10）是一种众所周知的抗脂肪形成因子，具有调节非酒精性脂肪肝疾病（NAFLD）的能力。但是，辅酶Q10对NAFLD起作用的机制仍不清楚。在这项研究中，在体内和体外研究了辅酶Q10在预防NAFLD中的作用。给C57BL / 6J小鼠喂食补充CoQ10（1800 mg kg ^-1）的正常饮食，高脂饮食（HFD）或HFDHFD）持续24周。HepG2细胞用棕榈酸钠处理以研究辅酶Q10对NAFLD的作用机理。结果表明，辅酶Q10通过降低血清甘油三酸酯，总胆固醇和低密度脂蛋白胆固醇水平，减轻了HFD诱导的体重增加和NAFLD，并具有抗高血脂症的作用。重要的是，辅酶Q10可能下调与脂质合成相关的固醇调节元件结合蛋白1c（SREBP-1c），乙酰辅酶A羧化酶（ACC）和脂肪酸合酶（FAS）的表达，并上调HQ10的表达。过氧化物酶体增殖物激活受体α（PPARα）和肉碱棕榈酰转移酶-1（CPT-1）与脂肪酸氧化有关。与小鼠的结果相似，辅酶Q10的治疗减轻了棕榈酸钠引起的肝细胞脂肪变性通过抑制脂肪生成和促进脂肪酸氧化。但是，化合物C作为AMPK抑制剂，可能会显着阻碍辅酶Q10治疗的益处。总之，辅酶Q10可以作为AMPK激活剂并调节肝脂质代谢，从而抑制肝脂质的异常蓄积并阻止NAFLD的发展。