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

Nutrition

Journal of Nutrition & Food Sciences

Author(s): Vlassara H, Cai W, Crandall J, Goldberg T, Oberstein R,

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Abstract Diet is a major environmental source of proinflammatory AGEs (heat-generated advanced glycation end products); its impact in humans remains unclear. We explored the effects of two equivalent diets, one regular (high AGE, H-AGE) and the other with 5-fold lower AGE (L-AGE) content on inflammatory mediators of 24 diabetic subjects: 11 in a 2-week crossover and 13 in a 6-week study. After 2 weeks on H-AGE, serum AGEs increased by 64.5\% (P = 0.02) and on L-AGE decreased by 30\% (P = 0.02). The mononuclear cell tumor necrosis factor-alphabeta-actin mRNA ratio was 1.4 +/- 0.5 on H-AGE and 0.9 +/- 0.5 on L-AGE (P = 0.05), whereas serum vascular adhesion molecule-1 was 1,108 +/- 429 and 698 +/- 347 ngml (P = 0.01) on L- and H-AGE, respectively. After 6 weeks, peripheral blood mononuclear cell tumor necrosis factor-alpha rose by 86.3\% (P = 0.006) and declined by 20\% (P, not significant) on H- or L-AGE diet, respectively; C-reactive protein increased by 35\% on H-AGE and decreased by 20\% on L-AGE (P = 0.014), and vascular adhesion molecule-1 declined by 20\% on L-AGE (P < 0.01) and increased by 4\% on H-AGE. Serum AGEs were increased by 28.2\% on H-AGE (P = 0.06) and reduced by 40\% on L-AGE (P = 0.02), whereas AGE low density lipoprotein was increased by 32\% on H-AGE and reduced by 33\% on L-AGE diet (P < 0.05). Thus in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury. Restriction of dietary AGEs suppresses these effects.
This article was published in Proc Natl Acad Sci U S A and referenced in Journal of Nutrition & Food Sciences

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