In summary, the present study clearly demonstrated that a
moderate level of dietary cholesterol (0.2% w/w) exacerbated simple
hepatic steatosis into NASH in HF-fed mice. Furthermore, our data
revealed the involvement of inflammation and retarded mitochondrial
function in the liver during this process but not oxidative stress or
ER stress. We also found, for the first time, that the blunted
mitochondrial function in the liver persisted after the inflammation
response and plasma ALT had subsided. These findings suggest that
cholesterol plays a critical role in the conversion of hepatic steatosis
toward NASH possibly by activation of inflammatory pathways along
with blunted mitochondrial function.