Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy - PubMed (original) (raw)
Clinical Trial
. 2002 Nov 26;99(24):15596-601.
doi: 10.1073/pnas.242407999. Epub 2002 Nov 12.
Affiliations
- PMID: 12429856
- PMCID: PMC137762
- DOI: 10.1073/pnas.242407999
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. 2002.
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.
Figures
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.
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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