Non-alcoholic fatty liver disease (
NAFLD) represents the result of hepatic fat overload not due to alcohol consumption and potentially evolving to advanced
fibrosis,
cirrhosis, and
hepatocellular carcinoma.
Fructose is a naturally occurring
simple sugar widely used in food industry linked to
glucose to form
sucrose, largely contained in hypercaloric food and beverages. An increasing amount of evidence in scientific literature highlighted a detrimental effect of dietary
fructose consumption on metabolic disorders such as
insulin resistance,
obesity, hepatic steatosis, and
NAFLD-related
fibrosis as well. An excessive
fructose consumption has been associated with
NAFLD development and progression to more clinically severe phenotypes by exerting various toxic effects, including increased
fatty acid production, oxidative stress, and worsening
insulin resistance. Furthermore, some studies in this context demonstrated even a crucial role in
liver cancer progression. Despite this compelling evidence, the molecular mechanisms by which
fructose elicits those effects on liver metabolism remain unclear. Emerging data suggest that dietary
fructose may directly alter the expression of genes involved in lipid metabolism, including those that increase hepatic fat accumulation or reduce hepatic fat removal. This review aimed to summarize the current understanding of
fructose metabolism on
NAFLD pathogenesis and progression.