Dietary Advanced Glycation End Products and Their Role in Health and Disease

Abstract

Over the past 2 decades there has been increasing evidence supporting an important contribution from food-derived advanced glycation end products (AGEs) to the body pool of AGEs and therefore increased oxidative stress and inflammation, processes that play a major role in the causation of chronic diseases. A 3-d symposium (1st Latin American Symposium of AGEs) to discuss this subject took place in Guanajuato, Mexico, on 1-3 October 2014 with the participation of researchers from several countries. This review is a summary of the different presentations and subjects discussed, and it is divided into 4 sections. The first section deals with current general knowledge about AGEs. The second section dwells on mechanisms of action of AGEs, with special emphasis on the receptor for advanced glycation end products and the potential role of AGEs in neurodegenerative diseases. The third section discusses different approaches to decrease the AGE burden. The last section discusses current methodologic problems with measurement of AGEs in different samples. The subject under discussion is complex and extensive and cannot be completely covered in a short review. Therefore, some areas of interest have been left out because of space. However, we hope this review illustrates currently known facts about dietary AGEs as well as pointing out areas that require further research.

Advanced Glycation End Products (Ages) in Food: Focusing on Mediterranean Pasta

“…Furthermore, AGE accumulation in collagen leads to changes in the biochemical and structural property of the components of the basement membrane affecting for example its elasticity, ionic charge, and thickness [50]. Accordingly, has been postulated that accumulation of AGE-crosslinking formed with vessel-wall collagen and basement membrane proteins, can contribute to vascular dysfunction [4,5]. In addition, AGE deposits have been found in atherosclerotic plaques and myocardium of patients with diabetes [2,52].…”

“…Recently, different studies on mice and human have demonstrated that dAGEs can be absorbed at intestinal level, and be potentially toxic [1,3,4].…”

“…Their toxic effects are essentially related to their ability to promote oxidative stress and inflammation by binding to cell surface receptors or cross-linking with body proteins, altering their structure and function [3,4].…”

Advanced Glycation Endproducts form During Ovalbumin Digestion in the Presence of Fructose

“…The authors suggest these three associations may be mediated through in situ enteral formation of fructose AGEs, which, after being absorbed, may contribute to inflammatory diseases via engagement of RAGE [15,[21][22][23]. Other food AGEs (preformed in cooking) have been shown to actually be absorbed and be pro-inflammatory in animal and human intervention studies [16]. They may participate in chronic inflammation enhancing insulin resistance in metabolic syndrome and diabetes as well as in renal failure [24][25][26] Given the ubiquity of ovalbumin and excess fructose in our diets, we reasoned that the possibility of an interaction between them during digestion needed exploration, especially in the light of the plausibility of this new hypothesis and our recent proof of principle study [27].…”

“…RAGE is involved in many inflammatory conditions [16][17][18][19]. RAGE is a pattern recognition receptor that binds AGE, among several ligands related to primary immunity [18][19].…”