Nonalcoholic fatty liver disease (NAFLD) is closely linked to diet quality and dysfunction of the gut–liver axis, including barrier failure, endotoxemia, and microbial dysbiosis. Heat processing generates advanced glycation end products (AGEs) abundant in modern foods, and higher intake associates with greater NAFLD risk, though causal evidence has been limited. Here we test whether a high-AGE diet (HAD) induces NAFLD-like pathology and whether resistant starch (RS) mitigates it via microbiome-mediated mechanisms. Prolonged HAD exposure caused hepatic triglyceride accumulation, dyslipidemia, impaired epithelial barrier function with elevated lipopolysaccharide, a microbiota shift toward proteolytic and opportunistic taxa, and transcriptomic signatures of disrupted lipid metabolism and inflammatory activation. Dietary AGEs foster a pro-inflammatory milieu by compromising barrier integrity, disturbing host–microbiome homeostasis, heightening cellular stress, and broadly amplifying innate immune activation. RS supplementation attenuated these changes by lowering hepatic lipid accumulation, restoring barrier integrity, reducing endotoxin burden, increasing short-chain fatty acids, and re-establishing saccharolytic/butyrogenic microbiota. A complementary in vitro colonic fermentation with a human fecal inoculum confirmed RS-driven acidification and accelerated turnover of N-acetylated intermediates, facilitating AGE detoxification and clearance. These findings provide experimental evidence that chronic dietary AGEs can initiate NAFLD-like pathology through disruption of the gut–liver axis and show that RS counters these effects by reprogramming microbial metabolism and strengthening intestinal barrier integrity.