LDLR and metabolic dysfunction-associated steatotic liver disease: Although the mechanisms of BER in the treatment of NAFLD are unclear, a variety of potential targeting pathophysiological processes has been proposed, including increase of hepatic insulin sensitivity [11], reduction of serum cholesterol by stabilizing mRNA of low density lipoprotein receptor (LDLR) [12], enhancement of mitochondrial function to reduce oxidative stress [13] and regulation on adenosine monophosphate activated protein kinase (AMPK) pathway [14].