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Glycation Damage: a Possible Hub for Major Pathophysiological Disorders and Aging

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Glycation Damage: a Possible Hub for Major Pathophysiological Disorders and Aging Volume 9, Number 5; 880-900, October 2018 http://dx.doi.org/10.14336/AD.2017.1121 Review Glycation Damage: A Possible Hub for Major Pathophysiological Disorders and Aging Maxime Fournet1, Frédéric Bonté2, Alexis Desmoulière3, * 1University of Limoges, Faculty of Pharmacy, Department of Physiology, EA 6309, F-87025 Limoges, France 2LVMH Recherche, F-45800 St-Jean-de-Braye, France 3University of Limoges, Faculty of Pharmacy, Department of Physiology, EA 6309, F-87025 Limoges, France [Received September 22, 2017; Revised November 21, 2017; Accepted November 21, 2017] ABSTRACT: Glycation is both a physiological and pathological process which mainly affects proteins, nucleic acids and lipids. Exogenous and endogenous glycation produces deleterious reactions that take place principally in the extracellular matrix environment or within the cell cytosol and organelles. Advanced glycation end product (AGE) formation begins by the non-enzymatic glycation of free amino groups by sugars and aldehydes which leads to a succession of rearrangements of intermediate compounds and ultimately to irreversibly bound products known as AGEs. Epigenetic factors, oxidative stress, UV and nutrition are important causes of the accumulation of chemically and structurally different AGEs with various biological reactivities. Cross-linked proteins, deriving from the glycation process, present both an altered structure and function. Nucleotides and lipids are particularly vulnerable targets which can in turn favor DNA mutation or a decrease in cell membrane integrity and associated biological pathways respectively. In mitochondria, the consequences of glycation can alter bioenergy production. Under physiological conditions, anti-glycation defenses are sufficient, with proteasomes preventing accumulation of glycated proteins, while lipid turnover clears glycated products and nucleotide excision repair removes glycated nucleotides. If this does not occur, glycation damage accumulates, and pathologies may develop. Glycation-induced biological products are known to be mainly associated with aging, neurodegenerative disorders, diabetes and its complications, atherosclerosis, renal failure, immunological changes, retinopathy, skin photoaging, osteoporosis, and progression of some tumors. Key words: exogenous glycation, endogenous glycation, advanced glycation end product, aging, neurodegenerative disorders, diabetes The French chemist, Louis-Camille Maillard, published subsequently studied these reactions including Amadori, an article in 1912 describing the changes that occur in at the end of the 1920s, and Hodge in the early 1950s. specific proteins once they attach to a sugar. This series of Glycated hemoglobin, discovered in 1955, was the first reactions known as the "Maillard reaction" is the main example of a molecule that had been altered by exposure reason why food develops color (browning) and aromas to blood sugar and provided proof that the Maillard when it is cooked (exogenous glycation). Maillard, a reaction also occurred in the human body (endogenous pioneering scientist, speculated that this reaction could glycation). Biologists now use the term glycation to play a role in a variety of fields, including physiology, describe the Maillard reaction in vivo. human pathology, and agronomy. Other scientists *Correspondence should be addressed to: Dr. Alexis Desmoulière, Service de physiologie et EA 6309, Faculté de Pharmacie, Université de Limoges, 2 rue du Docteur Marcland, 87025 Limoges cedex, France. E-mail address: [email protected]. Copyright: © 2017 Fournet M et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ISSN: 2152-5250 880 Fournet M., et al Glycation damage and aging Glycation is one of the fundamental mechanisms impact on health. In addition, nutrition during early involved in aging and is known to occur at different development plays an important role in susceptibility to reactive rates in young people compared to older people. disease in adult life. This suggests potential links between Moreover, glycation is also recognized to be more the nutrition status or diet and changes in gene expression associated with diabetes mellitus. While glycation that may lead to a predisposition to disease phenotypes products occur in healthy subjects and contribute to the [1]. The consumption of glycation products, especially aging process, long-term hyperglycemia, in diabetic those formed during cooking, could also be potentially subjects, results in an increase in these products, harmful to our health. triggering toxic mechanisms that have a more serious Figure 1. In vivo glycation processes. General mechanisms of exogenous and endogenous glycation is the result of a covalent bond between a glycation carbonyl group from a reducing sugar (aldose or ketose) and a free amino group. Through a reversible reaction, Glycation is a non-enzymatic reaction that occurs between exogenous glycation forms a Schiff base after the a carbohydrate and a molecule with a free amino group, liberation of a water molecule. After the Schiff base is such as a protein (Fig. 1). This irreversible and cumulative irreversibly isomerised, Amadori products are formed reaction takes place spontaneously in the body. All from aldoses and Heyns-Carson products are formed from resulting metabolic intermediates are then reactive. ketoses. Once these products fragment, in a process Glycation is a physiological and pathological process that known as the retro-aldol reaction, they create a series of produces so-called glycated proteins and is entirely aldehydes and carbonyl compounds including separate from glycosylation, which represents an enzyme- glyceraldehyde, formaldehyde, and glyoxal, which in turn controlled physiological process that occurs during can react with another amino group. The compounds synthesis of glycoproteins. When it occurs outside of the formed by splitting these products include important body, glycation is responsible for the browning process intermediary molecules that are also created during that occurs in food during cooking [2]. Exogenous endogenous glycation; these are known as glycation Aging and Disease • Volume 9, Number 5, October 2018 881 Fournet M., et al Glycation damage and aging intermediaries. Glycation intermediaries can continue to hyperglycemia. The body's proteins thus come into react, creating advanced glycation end products, or AGEs contact with high levels of blood sugar (chronic (Fig. 1). AGEs refer to the end products formed by hyperglycemia). As a result, glycation is accelerated and endogenous glycation. An AGE, such as N-ε- contributes to the various complications associated with carboxymethyl-lysine (CML) or N-ε-carboxyethyl-lysine diabetes [4-6]. The resulting carbonyl molecules tend to (CEL), can also form during exogenous glycation and be accumulate in the bodies of subjects suffering from present in food [3]. diabetes or from kidney failure [7-10]. Endogenous physiological glycation involves These intermediaries are very reactive and cause glucose, the body's most prevalent reducing sugar, and the carbonyl stress, which in turn can aggravate inflammation functions of free amino groups present in the body as well, and oxidative stress. especially amino acids in proteins like lysine and arginine. The reactive intermediaries described above are It has also been shown to play a role in numerous located at the "crossroads" of various metabolic pathways. pathologies in diabetic and non-diabetic patients alike. The polyol, glycolysis, glucose autoxidation, and lipid Glycation increases in patients with type I diabetes due to peroxidation pathways create these same glycation pancreatic beta cell failure and the consequent loss of intermediaries (Fig. 2). control of blood glucose which leads to hyperglycemia. In type II diabetes, insulin resistance similarly results in Figure 2. All AGEs formed in the body due to glycation and four other metabolic pathways. Once formed, these intermediaries react, just as they products formed by the pathways mentioned above. This would during the glycation process, with amino acids in is also why AGEs have a variable "pathological proteins such as lysine, to produce AGEs (CML, CEL, or expression" in diabetes mellitus, kidney failure, and tissue pyrraline) without previously undergoing glycation. It is aging. Aminophospholipids, which are found in cellular for this reason that the term AGE strictly refers to all and mitochondrial membranes, phosphatidyl- AGEs produced through glycation, plus the advanced end ethanolamines, and serines are present in vivo in a Aging and Disease • Volume 9, Number 5, October 2018 882 Fournet M., et al Glycation damage and aging glycated form. The resulting structural changes affect many organs including skin, means that a complete phase transitions, which in turn alters membrane glycation reaction can occur, resulting in the formation of plasticity, membrane potential, and conductance. The pro- AGEs [20, 21]. The reactivity of carbohydrates decreases oxidative role of the glycated forms is also associated with as their size increases. Pentoses are thus more reactive cellular responses such as the activation of the than hexoses. The low reactivity of the carbohydrates transcription factor nuclear factor-B (NF-B). They also most commonly found in humans is due to their extremely
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