Main |
Browse Volumes |
Forthcoming Volumes |
Annals PrePrints |
Annals Extra |
E-mail Alerts |
Subscriptions & Orders |
New Proposals |
Author Guidelines |
About Annals |
Help |
 |
|
|
|
|
|
Advanced Glycation in Health and Disease: Role of the Modern Environment
HELEN VLASSARA
Division of Experimental Diabetes and Aging, Brookdale Department of Geriatrics and Adult Development, Mount Sinai School of Medicine, New York, New York 10029, USA
Address for correspondence: Helen Vlassara, M.D., Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029. Voice: 212-241-2567; fax: 212-241-7248. helen.vlassara{at}mssm.edu
It is believed that intracellular and extracellular advanced glycation (AGEs) or lipoxidation end products (ALEs), together with dysregulated glucose and lipid metabolism, are important contributors to oxidant or carbonyl stress, enhanced cellular redox-sensitive transcription factor activity, and impaired innate immune defense, causing over time inappropriate inflammatory responses. However, neither the magnitude nor the persistent nature of this increased prooxidant state are completely understood. A significant correlation has been found between ingested and circulating AGEs in humans in recent years. Based on animal studies, the injurious impact of diet-derived AGEs to vascular and kidney tissues is estimated to rival or even exceed that caused by hyperglycemia or hyperlipidemia. Consistent with this view, dietary AGE restriction has been associated with suppression of several immune defects, insulin resistance, and diabetic complications, whether genetically or diet induced, despite persistent diabetes. These findings are in support of clinical evidence from subjects with diabetes or vascular or kidney disease. Most recently, evidence from animal studies points to AGE restriction as an effective means for extending median life span, similar to that previously shown by marked caloric restriction. We conclude that excessive AGE consumption, in the current dietary/social structure, represents an independent factor for inappropriate oxidant stress responses, which may promote the premature expression of complex diseases associated with adult life, such as diabetes and cardiovascular disease.
Key Words: glycotoxins • oxidation • lipoxidation • innate immunity • insulin resistance • cardiovascular disease • kidney disease • AGE restriction • caloric restriction
This article has been cited by other articles:
|
|
|
|
 
H. VLASSARA, J. URIBARRI, W. CAI, and G. STRIKER
Advanced Glycation End Product Homeostasis: Exogenous Oxidants and Innate Defenses
Ann. N.Y. Acad. Sci.,
April 1, 2008;
1126(1):
46 - 52.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. KUEPER, T. GRUNE, G.-M. MUHR, H. LENZ, K.-P. WITTERN, H. WENCK, F. STAB, and T. BLATT
Modification of Vimentin: A General Mechanism of Nonenzymatic Glycation in Human Skin
Ann. N.Y. Acad. Sci.,
April 1, 2008;
1126(1):
328 - 332.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Bengmark
Advanced Glycation and Lipoxidation End Products-Amplifiers of Inflammation: The Role of Food
JPEN J Parenter Enteral Nutr,
September 1, 2007;
31(5):
430 - 440.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Kueper, T. Grune, S. Prahl, H. Lenz, V. Welge, T. Biernoth, Y. Vogt, G.-M. Muhr, A. Gaemlich, T. Jung, et al.
Vimentin Is the Specific Target in Skin Glycation: STRUCTURAL PREREQUISITES, FUNCTIONAL CONSEQUENCES, AND ROLE IN SKIN AGING
J. Biol. Chem.,
August 10, 2007;
282(32):
23427 - 23436.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Negrean, A. Stirban, B. Stratmann, T. Gawlowski, T. Horstmann, C. Gotting, K. Kleesiek, M. Mueller-Roesel, T. Koschinsky, J. Uribarri, et al.
Effects of low- and high-advanced glycation endproduct meals on macro- and microvascular endothelial function and oxidative stress in patients with type 2 diabetes mellitus
Am. J. Clinical Nutrition,
May 1, 2007;
85(5):
1236 - 1243.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Liu, F. Zheng, Z. Li, J. Uribarri, B. Ren, R. Hutter, J. R. Tunstead, J. Badimon, G. E. Striker, and H. Vlassara
Reduced Acute Vascular Injury and Atherosclerosis in Hyperlipidemic Mice Transgenic for Lysozyme
Am. J. Pathol.,
July 1, 2006;
169(1):
303 - 313.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. G. Huebschmann, J. G. Regensteiner, H. Vlassara, and J. E.B. Reusch
Diabetes and Advanced Glycoxidation End Products.
Diabetes Care,
June 1, 2006;
29(6):
1420 - 1432.
[Full Text]
[PDF]
|
|
|
|
