Non-alcoholic fatty liver disease (NAFLD) affects a significant portion of the adult population and is a leading cause of liver-related illness and mortality worldwide. Treatment mainly relies on lifestyle changes, which can be challenging for most patients. The progression from simple fatty liver to more severe forms, such as non-alcoholic steatohepatitis (NASH) and liver fibrosis, is explained by a “two-hit hypothesis.” Advanced glycation end products (AGEs), formed when sugars react with proteins or lipids, have emerged as major contributors to this second hit, driving the progression from steatosis to NASH through the receptor for AGEs (RAGE). Both endogenous and exogenous AGEs from processed foods can activate RAGE in specific liver cells, promoting NAFLD progression. This review focuses on the pathophysiology of NAFLD, highlighting the role of food-derived AGEs in the development of NASH and liver fibrosis. Additionally, the potential impact of dietary changes to reduce AGEs in food or therapies targeting the AGE/RAGE pathway on disease progression is discussed.
NAFLD affects a large portion of the population and is a major cause of liver-related illness and deaths. The progression from fatty liver to NASH is driven by advanced glycation end products (AGEs) acting through the RAGE receptor. Both endogenous and exogenous AGEs contribute to NAFLD progression. This review focuses on the role of food-derived AGEs in NASH and liver fibrosis and discusses dietary modifications and therapies targeting the AGE/RAGE pathway.
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