Dietary advanced glycation end‐products: Perspectives linking food processing with health implications

Abstract

Dietary advanced glycation end products (dAGEs) are complex and heterogeneous compounds derived from nonenzymatic glycation reactions during industrial processing and home cooking. There is mounting evidence showing that dAGEs are closely associated with various chronic diseases, where the absorbed dAGEs fuel the biological AGEs pool to exhibit noxious effects on human health. Currently, due to the uncertain bioavailability and rapid renal clearance of dAGEs, the relationship between dAGEs and biological AGEs remains debatable. In this review, we provide the most updated information on dAGEs including their generation in processed foods, analytical and characterization techniques, metabolic fates, interaction with AGE receptors, implications on human health and reducing strategies. Available evidence demonstrating a relevance between dAGEs and food allergy is also included. AGEs are ubiquitous in foods and their contents largely depend on the reactivity of carbonyl and amino groups, along with surrounding condition mainly pH and heating procedures. Once being digested and absorbed into the circulation, two separate pathways can be involved in the deleterious effects of dAGEs: an AGE receptor‐dependent way to stimulate cell signals, and an AGE receptor‐independent way to dysregulate proteins via forming complexes. Inhibition of AGEs formation during food processing and reduction in the diet are two potent approaches to restrict health‐hazardous dAGEs. To elucidate the biological role of dAGEs toward human health, the following significant perspectives are raised: molecular size and complexity of dAGEs; interactions between unabsorbed dAGEs and gut microbiota; and roles played by concomitant compounds in the heat‐processed foods.

Can the Consumption of Ultra-Processed Food Be Associated with Anthropometric Indicators of Obesity and Blood Pressure in Children 7 to 10 Years Old?

“…AGEs are heterogeneous compounds derived from non-enzymatic glycation reactions from interactions between reducing sugars or oxidized lipids and proteins or nucleic acids. The pathological effects of AGEs are related to their ability to alter the chemical and functional properties of proteins and activate intracellular pathways promoting oxidative stress [78,79]. Studies indicate the possible effect of dietary AGEs on inflammation and cardiometabolic dysfunction in adults and in the pediatric population [80][81][82].…”

Diet-Derived Antioxidants and Their Role in Inflammation, Obesity and Gut Microbiota Modulation

“…), and they contribute in altering cellular functioning [ 66 ]. Through the RAGEs receptor, they activate NFkB, a cellular mediator of inflammation [ 67 ], thus stimulating and supporting the inflammatory process.…”

“…The major sources of AGEs are grilled meats, baked goods, dairy products and processed food in general: high circulating levels of them are linked to oxidative stress and inflammation, which promote aging [ 68 ]. Fruits, vegetables and whole grains appear to have less AGEs [ 67 ].…”

Dietary AGEs as Exogenous Boosters of Inflammation

“…Nonetheless, there is controversy on whether these reactive compounds could contribute to AGE burden, since other researchers have shown that dietary dicarbonyls are unlikely to directly contribute to the endogenous pool of these compounds [ 85 ]. It has also been suggested that high-fat diets induce in vivo dicarbonyl formation [ 85 , 86 ]. Therefore, the increased level of endogenous AGEs observed in in vivo studies offering a roasted, high-fat diet might be partially explained by the high-fat induced formation of dicarbonyl compounds.…”