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Clinical Trial
.2002 Nov 26;99(24):15596-601.
doi: 10.1073/pnas.242407999. Epub 2002 Nov 12.

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

Affiliations
Clinical Trial

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

Helen Vlassara et al. Proc Natl Acad Sci U S A..

Erratum in

  • Proc Natl Acad Sci U S A. 2003 Jan 21;100(2):763.

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.

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Figures

Fig. 1.
Fig. 1.
Circulating AGE levels correspond to dietary AGE intake: a randomized 6-week study. Fasting sAGE levels were determined in 13 diabetic patients (H-AGE,n = 6; L-AGE,n = 7) by CML-sensitive (A) (4G9 mAb) or an MG derivative-sensitive ELISA (B) (3D11 mAb). (C) Plasma AGE-LDL lipid levels were assessed by direct ELISA (4G9). Values are shown at baseline (BL) and the end of H-AGE or L-AGE; data are shown as mean ± SEM of triplicate measurements. The percentage of change between H-AGE and L-AGE are shown (Right). *,P < 0.05; **,P < 0.01.
Fig. 2.
Fig. 2.
Changes in circulating inflammatory markers during a 6-week exposure to H-AGE versus L-AGE diet: a randomized study. Serum CRP (A), peripheral blood mononuclear cell-derived TNFα (B), or serum VCAM-1 values (C) were obtained at baseline (BL) or at the end of H-AGE or L-AGE periods; data are shown as mean ± SEM of triplicate measurements (n = 13 patients: H-AGE,n = 6; L-AGE,n = 7). The percent changes between H-AGE and L-AGE are displayed (Right). *,P < 0.05; **,P < 0.01.
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References

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