Evidence map›Paper›PMID 12429856›Full record

Trial reportProceedings of the National Academy of Sciences of the United States of America2002

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

Helen Vlassara, Weijing Cai, Jill Crandall, Teresia Goldberg, Robert Oberstein, Veronique Dardaine, Melpomeni Peppa, Elliot J Rayfield

Erratum issuedOpen access · bronzeAbstract readClinical TrialComparative StudyRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 211 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
211citing papers in PubMed, 10 pooled it
15.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

211 citing papers in PubMed, 10 syntheses or guidelines pooled it, 663 citations in OpenAlex.

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  10. Intake of sugar-sweetened beverages and weight gain: a systematic review.The American journal of clinical nutrition · 2006
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151 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Helen VlassaraDivision of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA. helen.vlassara@mssm.edu
Weijing Cai
Jill Crandall
Teresia Goldberg
Robert Oberstein
Veronique Dardaine
Melpomeni Peppa
Elliot J Rayfield
Icahn School of Medicine at Mount Sinai · US

Funding

ZIPRASIDONE (GEODON) AUGMENTATION IN SEROTONIN REUPTAKE INHIBITOR-RESISTANT OBM01RR000071 · NCRR · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI OHNUMA, TAKAO · 1985 to 2009
$41.5M
AGING &VASCULAR DISEASE ROLE OF GLYCATIONR01AG009453 · NIA · PICOWER INSTITUTE FOR MEDICAL RESEARCH · PI VLASSARA, HELEN · 1991 to 2007
$2.6M
NCRR NIH HHS MO1-RR-00071NIA NIH HHS AG09453NIA NIH HHS R01 AG009453
6 · The paper itself

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.

Indexed as

BiomarkersC-Reactive ProteinCross-Over StudiesDiabetes ComplicationsDiabetes MellitusDiabetic AngiopathiesDietDietary CarbohydratesDietary FatsDietary ProteinsFemaleFood AnalysisFood, FormulatedGene Expression RegulationGlycation End Products, AdvancedHumansBiomarkersC-Reactive ProteinDietary CarbohydratesDietary FatsDietary ProteinsGlycation End Products, AdvancedInflammation MediatorsLysineN(6)-carboxymethyllysinePyruvaldehydeTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID12429856
PMCPMC137762
OpenAlexW2159634370

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.