Abstract
Background: High levels of glycated and lipoxidated proteins and peptides in the body are repeatedly associated with chronic diseases. These molecules are strongly associated with activation of a specific receptor called RAGE and a long-lasting exaggerated level of inflammation in the body. Methods: PubMed reports over 5000 papers plus >13,500 articles about the related HbA1c, most of them published in the past 5 years. Most of the available abstracts have been read and approximately 800 full papers have been studied. Results: RAGE, a member of the immunoglobulin superfamily of cell surface molecules and receptor for advanced glycation end products, known since 1992, functions as a master switch, induces sustained activation of nuclear factor κB (NFκB), suppresses a series of endogenous autoregulatory functions, and converts long-lasting proinflammatory signals into sustained cellular dysfunction and disease. Its activation is associated with high levels of dysfunctioning proteins in body fluids and tissues, and is strongly associated with a series of diseases from allergy and Alzheimers to rheumatoid arthritis and urogenital disorders. Heat treatment, irradiation, and ionization of foods increase the content of dysfunctioning molecules. Conclusions: More than half of the studies are performed in diabetes and chronic renal diseases; there are few studies in other diseases. Most of our knowledge is based on animal studies and in vitro studies. These effects are worth further exploration both experimentally and clinically. An avoidance of foods rich in deranged proteins and peptides, and the consumption of antioxidants, especially polyphenols, seem to counteract such a development.
Nonenzymatic reactions in the body and in the food we eat result in glycation and lipoxidation of proteins and peptides. Such abnormal molecules will accumulate in the body and induce inflammation. Numerous diseases are associated with high levels serum and tissue levels of such deranged substances. Clinical studies are warranted.
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