Advanced Glycation in Health and Disease: Role of the Modern Environment

  title={Advanced Glycation in Health and Disease: Role of the Modern Environment},
  author={Helen Vlassara},
  journal={Annals of the New York Academy of Sciences},
  • H. Vlassara
  • Published 1 June 2005
  • Medicine, Biology
  • Annals of the New York Academy of Sciences
Abstract: 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… 

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Advanced Glycation End Product Homeostasis

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[Advanced glycation and lipoxidation end products--amplifiers of inflammation: the role of food].

Continous intake of AGE and ALE contributes to the exccesive accumulation of these products into body tissues, which in turn negatively influence the innate immune system, inflammatory responses, and resistance to diseases.

Current perspectives on the health risks associated with the consumption of advanced glycation end products: recommendations for dietary management

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The Role of Advanced Glycation End-Products in Cancer Disparity.

  • D. Turner
  • Biology
    Advances in cancer research
  • 2017

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This chapter described some possible solutions and health guidelines for consumers against deleterious effects represented by advanced glycation products, including microbiological causes and effects, chemical and physical features, and technological factors linked to the First and the Second Laws of Food Degradation.



Glycoxidation and Diabetic Complications: Modern Lessons and a Warning?

Evidence is reviewed which suggests that the elevated oxidative stress resulting from chronic hyperglycemia may not occur in a vacuum, but rather in an internal environment already oxidatively “primed,” due to constant exposure to a steady stream of AGE-modified food substances consumed since infancy.

Role of oxidative stress in diabetic complications: a new perspective on an old paradigm.

It is proposed that the increased chemical modification of proteins by carbohydrates and lipids in diabetes is the result of overload on metabolic pathways involved in detoxification of reactivecarbonyl species, leading to a general increase in steady-state levels of reactive carbonyl compounds formed by both oxidative and nonoxidative reactions.

Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy

In diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury, and Restriction of dietary A GEs suppresses these effects.

Orally absorbed reactive glycation products (glycotoxins): an environmental risk factor in diabetic nephropathy.

The renal excretion of orally absorbed AGEs is markedly suppressed in diabetic nephropathy patients, daily influx of dietary A GEs includes glycotoxins that may constitute an added chronic risk for renal-vascular injury in DM, and dietary restriction of AGE food intake may greatly reduce the burden of AAGEs in diabetic patients and possibly improve prognosis.

Oxidative Stress-Inducing Carbonyl Compounds From Common Foods: Novel Mediators of Cellular Dysfunction

Food-derived AGE, prior to absorption, contain potent carbonyl species, that can induce oxidative stress and promote inflammatory signals, similar to native AGEs.

The AGE‐receptor in the pathogenesis of diabetic complications

  • H. Vlassara
  • Biology, Medicine
    Diabetes/metabolism research and reviews
  • 2001
Though several gene polymorphisms are detected in most AGE‐R components, no significant correlation to diabetic complications has as yet been found, and further investigation is underway to define whether primary or secondary genetic links of pathogenic significance exist in this system.

Restriction of dietary glycotoxins reduces excessive advanced glycation end products in renal failure patients.

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Glycoxidation and inflammation in renal failure patients.

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Advanced glycation end-products: a review

The chemistry of advanced glycated end-product formation and their patho-biochemistry particularly in relation to the diabetic microvascular complications of retinopathy, neuropathy and nephropathy as well as their role in the accelerated vasculopathy observed in diabetes are discussed.