Dietary Advanced Glycation End Products (AGEs) are bioactive compounds formed during high-temperature cooking methods such as frying, grilling, and roasting. In addition to their endogenous production under hyperglycemic and oxidative conditions, exogenous AGEs from food are increasingly recognized as contributors to gastrointestinal dysfunction and liver pathology. Through mechanisms involving oxidative stress, low-grade chronic inflammation, intestinal barrier disruption, and alterations in gut microbiota, dietary AGEs may play a crucial role in the development and progression of disorders such as irritable bowel syndrome (IBS), increased gut permeability, and non-alcoholic fatty liver disease (NAFLD). Considering the global rise of digestive and metabolic diseases, understanding the impact of AGEs on the gut–liver axis is clinically relevant.

A systematic review was conducted following PRISMA guidelines. PubMed, Scopus, and Web of Science were searched for studies published between 2010 and 2024 examining the impact of dietary (exogenous) AGEs on gastrointestinal and liver outcomes. Search terms included: “dietary AGEs,” “advanced glycation end products,” “gut permeability,” “intestinal inflammation,” “gut microbiota,” “liver disorders,” and “NAFLD.” Peer-reviewed original studies, including observational studies, clinical trials assessing dietary AGE intake, and animal or in-vitro studies with exogenous AGEs, were included. Studies focusing exclusively on endogenous AGEs, review articles, conference abstracts, and papers lacking full text were excluded. Key information was extracted, including study type, method of AGE assessment, gastrointestinal or liver outcomes, and main results. Due to heterogeneity in study designs and outcomes, results were summarized qualitatively.

Evidence from human and animal studies consistently indicates that high dietary AGEs intake is associated with impaired gut barrier function, altered gut microbiota, and increased intestinal inflammation, marked by elevated pro-inflammatory cytokines such as TNF-α and IL-6. In the liver, excessive dietary AGEs contribute to hepatic fat accumulation, oxidative stress, and activation of the RAGE signaling pathway, promoting inflammation and fibrotic processes. Observational human studies show a positive association between high dietary AGEs and risk of NAFLD, while mechanistic animal studies confirm causal links between dietary AGEs, increased gut permeability, and liver injury. Although endogenous AGEs contribute to systemic inflammation and metabolic stress, their impact on gastrointestinal and hepatic outcomes appears secondary to dietary AGEs.

This review emphasizes that dietary AGEs exert a direct and significant effect on gut and liver health. Disruption of gut microbial balance and intestinal inflammation may facilitate translocation of microbial products to the liver, activating the RAGE pathway and inducing oxidative stress, inflammation, and fibrosis. Reducing dietary AGE intake, particularly from high-heat cooked and processed foods, may represent a practical preventive strategy. Future research should clarify dose-response relationships, long-term effects, and interactions between dietary and endogenous AGEs. Overall, these findings underscore the critical role of dietary AGEs in the gut–liver axis and support the integration of targeted dietary strategies into preventive and therapeutic approaches for gastrointestinal and liver diseases.