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.