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.