Introduction: Diet plays a crucial role in triggering deleterious physiological responses. Dietary Advanced glycation end-products (dAGEs) are suggested to lead to chronic low-grade inflammation (CLGI), oxidative stress, and alter gut bacteria. Studies investigate how glycation products like dietary carboxymethyl-lysine (dCML) and the Receptor for Advanced Glycation End-Products (RAGE) affect cellular responses, but it is unclear if early-life or lifelong exposure to dAGEs could contribute cited consequences of AGE intake, and whether these effects can be reversed. Materials and methods: Our study employed standard and an in-house prepared protein-dCML model to enrich mice food and explored how a high (13-times) dCML-enriched diet affects Wild-Type (WT) and RAGE KO mice from birth to 6, 35, and 70 weeks. We also investigated if switching to a standard diet at 6-weeks of age could reverse the potential dCML effects in the “Switch group”. We assessed outcomes at systemic and local levels using quantitative (LC-MS/MS) and molecular biology methods (qRT-PCR, Metagenomics) to quantify dCML and physiological changes, respectively, in multiple organs. Results: We confirmed the accumulation of free dCML in kidneys (3x), ileum (17x), and colon (20x) from 6 to 70 weeks of diet, regardless of RAGE expression. Switching diets lowered dCML comparable control conditions. The dCML-enrich diet did not notably affect endogenous glycation, inflammation, or senescence. TNFα, VCAM1, IL6, and P16 gene expression roughly doubled with age, especially in WT kidneys. There were notable increases in TNFα expression detected in the intestinal tract of the Switch group, suggesting an increased inflammatory reaction that could be related to timing of dietary shifts. Minor alterations in gut microbiota communities were observed. Discussion and conclusion: While persistent intake of dCML resulted in increased free dCML levels within tissues, there were no notable increases in parameters associated with inflammageing, oxidative stress, or significative microbial community shifts. However, early-life diet switching seemed to contribute with greater sensitivity to intestinal inflammation and increased TNFα expression. In addition, the lack of RAGE seemed to lower age-related TNFα increase in a healthy rodent model. It provides a potential avenue for future research to delve into understanding the influence of dAGEs on the onset of different diseases and health conditions.