![]() Low dAGE intake has also been shown to lengthen lifespan to the same extent as does energy restriction in mice ( 16). On the other hand, restriction of dAGEs prevents vascular and kidney dysfunction ( 18, 19), diabetes type 1 or type 2 ( 20), improves insulin sensitivity ( 21, 22), and accelerates wound healing ( 23). However, recent studies with the oral administration of a single AGE-rich meal to human beings as well as labeled single protein-AGEs or diets enriched with specific AGEs such as MG to mice clearly show that dAGEs are absorbed and contribute significantly to the body’s AGE pool ( 14– 16).Ĭonsumption of AGE-rich diets by mice is associated with elevated circulating and tissue AGEs and conditions such as atherosclerosis ( 17) and kidney disease ( 18). Because it had previously been assumed that dietary AGEs (dAGEs) are poorly absorbed, their potential role in human health and disease was largely ignored. The fact that the modern diet is a large source of AGEs is now well-documented ( 3, 7, 13). ![]() A wide variety of foods in modern diets are exposed to cooking or thermal processing for reasons of safety and convenience as well as to enhance flavor, color, and appearance. In particular, grilling, broiling, roasting, searing, and frying propagate and accelerate new AGE formation ( 7, 13). AGEs are naturally present in uncooked animal-derived foods, and cooking results in the formation of new AGEs within these foods. In addition to AGEs that form within the body, AGEs also exist in foods. Both these AGEs can be derived from protein and lipid glycoxidation ( 11, 12). Among the better-studied AGEs are the stable and relatively inert N ε-carboxymethyllysine (CML) and the highly reactive derivatives of methyl-glyoxal (MG). The pathologic effects of AGEs are related to their ability to promote oxidative stress and inflammation by binding with cell surface receptors or cross-linking with body proteins, altering their structure and function ( 8– 10). The formation of AGEs is a part of normal metabolism, but if excessively high levels of AGEs are reached in tissues and the circulation they can become pathogenic ( 2). This reaction is also known as the Maillard or browning reaction ( 7). AGEs are created through a nonenzymatic reaction between reducing sugars and free amino groups of proteins, lipids, or nucleic acids. The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake.Īdvanced glycation end products (AGEs), also known as glycotoxins, are a diverse group of highly oxidant compounds with pathogenic significance in diabetes and in several other chronic diseases ( 1– 6). ![]() The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. Animal-derived foods that are high in fat and protein are generally AGE-rich and prone to new AGE formation during cooking. Based on the findings, dry heat promotes new dAGE formation by >10- to 100-fold above the uncooked state across food categories. This report significantly expands the available dAGE database, validates the dAGE testing methodology, compares cooking procedures and inhibitory agents on new dAGE formation, and introduces practical approaches for reducing dAGE consumption in daily life. Dietary advanced glycation end products (dAGEs) are known to contribute to increased oxidant stress and inflammation, which are linked to the recent epidemics of diabetes and cardiovascular disease. Modern diets are largely heat-processed and as a result contain high levels of advanced glycation end products (AGEs).
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