Effect of diet-derived advanced glycation end products on inflammation

Abstract

Advanced glycation end products (AGEs) formed via the Maillard reaction during the thermal processing of food contributes to the flavor, color, and aroma of food. A proportion of food-derived AGEs and their precursors is intestinally absorbed and accumulates within cells and tissues. AGEs have been implicated in the pathogenesis of diabetes-related complications and several chronic diseases via interaction with the receptor for AGEs, which promotes the transcription of genes that control inflammation. The dicarbonyls, highly reactive intermediates of AGE formation, are also generated during food processing and may incite inflammatory responses through 1) the suppression of protective pathways, 2) the incretin axis, 3) the modulation of immune-mediated signaling, and 4) changes in gut microbiota profile and metabolite sensors. In animal models, restriction of dietary AGEs attenuates chronic low-grade inflammation, but current evidence from human studies is less clear. Here, the emerging relationship between excess dietary AGE consumption and inflammation is explored, the utility of dietary AGE restriction as a therapeutic strategy for the attenuation of chronic diseases is discussed, and possible avenues for future investigation are suggested.