Non-alcoholic fatty liver disease (NAFLD), a growing health issue around the world, is defined as
the presence of steatosis in the liver without any other detectable byproducts such as alcohol consumption,
which includes a wide spectrum of pathologies, such as steatohepatitis, cirrhosis, and hepatocellular carcinoma.
A growing body of evidence indicates that the reduction in the 5' adenosine monophosphate-activated protein
kinase (AMPK) activity, which could be activated by the consumption of the drugs, hormones, cytokines, and
dietary restriction, is related to some metabolic disorders such as obesity, diabetes, PCOS, and NAFLD. Vanillic
acid (VA), as an anti-inflammatory, anti-oxidative, anti-angiogenic and anti-metastatic factor, has protective
effects on the liver as in two animal models of liver damage, it reduces serum levels of transaminases, inflammatory
cytokines, and the accumulation of collagen in the liver and also prevents liver fibrosis. Besides, it decreases
body and adipose tissue weight in a mice model of obesity and, similar to the liver tissue, diminishes
adipogenesis through the activation of AMPK. It has been reported that VA can target almost all of the metabolic
abnormalities of NAFLD, such as hepatic steatosis, inflammation, and hepatic injury, at least partially
through the activation of AMPK. Therefore, in this review, we will discuss the possible and hypothetical roles
of VA in NAFLD, with a special focus on AMPK.