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Full Description
This book focuses on two major multidisciplinary topics on the Maillard reaction, that is food science and medical science. The former covers the reaction mechanism and kinetics and analytical aspect of the Maillard reaction, food technology, flavour chemistry, ecology and antioxidants, whereas the latter covers in vivo reaction of the Maillard reaction affecting human health and disease with a special focus on the significance of AGE in AGE-induced disease processes. Recent studies demonstrated that AGE concentration, adjusted for age and duration of diabetes, is also increased in diabetic patients with complications, including nephropathy, retinopathy, and atherosclerosis. AGE is also recognized by AGE receptor such as RAGE (receptor for AGE) and scavenger receptor type I and II. Furthermore, the AGE inhibitors, aminoguanidine and pyridoxamine, also inhibit AGE formation and retard the development of early renal disease in the streptozotocin-diabetic rat. Considered together, these studies strongly suggest an association between AGE and the development of diabetic complications.
Contents
Preface. Special memorial lecture. An approach to estimate the chemical structure of melanoidins (H. Kato, F. Hayase). The prospects of health and longevity from the inhibition of the Maillard reaction in vivo (V.M. Monnier et al.). Plenary sessions. Dysfunction of antioxidative enzymes and redox regulation under nitrosative stress and glycoxidative stress (Y. Miyamoto et al.). Pyridoxamine, a versatile inhibitor of advanced glycation and lipoxidation reactions (J. W. Baynes). The "colorful" chemistry of nonezymatic browning (T. Hofmann, O. Frank). Luncheon seminar. The role of AGE-RAGE system in the development of diabetic nephropathy in vivo (Y. Yamamoto et al.). Oral sessions - medical science. Formation of N-(carboxymethyl)lysine in inflammatory and non-inflammatory conditions of nerve and muscle and in inflammatory cells in vitro (E. Schleicher et al.). Amadori-glycated phosphatidylethanolamine induces lipid peroxidation in membrane model (M. Yamada et al.). Cellular oxidant stress mediated by advanced glycation endproducts: the role of native albania (R. Subramaniam et al.). Formation of pathways of N-(carboxymethyl)lysine and dicarbonyl compounds by peroxynitrite (Y. Unno et al.). Human serum albumin minimally modified by methylglyoxal binds to human mononuclear leukocytes via the RAGE receptor and is displaced by N-carboxymethyl-lysine and hydroimidazolone AGE epitopes (R. Ng et al.). Methylglyoxal induces apoptosis in rat mesangial cells (B.-F. Liu et al.). Activation of MAP kinase superfamily signaling pathways by methylglyoxal (S. Miyata et al.). CML: a brief history (S.R. Thorpe, J.W. Baynes). Inhibition of the development of experimental diabetic neuropathy by suppression of AGE formation with a new antiglycation agent (R. Wada et al.). Novel anit-glycation therapeutic agents: glyoxalase I mimetics (S. Battah, N. Ahmed, P.J. Thornalley). New horizons in age research (R. Buc
