Evidence map›Paper›PMID 21610689›Full record

ReviewNature reviews. Endocrinology2011

AGE restriction in diabetes mellitus: a paradigm shift.

Helen Vlassara, Gary E Striker

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 3 pooled it
10.2field-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

130 citing papers in PubMed, 3 syntheses or guidelines pooled it, 265 citations in OpenAlex.

  1. Host insulin resistance caused byFrontiers in cellular and infection microbiology · 2023
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Trial
  11. Trial
  12. Trial
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

70 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Helen VlassaraDivision of Experimental Diabetes and Aging, Brookdale Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA. helen.vlassara@ mssm.edu
Gary E Striker
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 NEWCORN, JEFFREY H · 1985 to 2009
$41.5M
Effects of Glycoxidative Stress on Human AgingR01DK091231 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2010 to 2014
$3.1M
NCRR NIH HHS M01 RR000071NCRR NIH HHS RR‑00071NIDDK NIH HHS DK091231NIDDK NIH HHS R01 DK091231
6 · The paper itself

Abstract

Persistently elevated oxidative stress and inflammation precede or occur during the development of type 1 or type 2 diabetes mellitus and precipitate devastating complications. Given the rapidly increasing incidence of diabetes mellitus and obesity in the space of a few decades, new genetic mutations are unlikely to be the cause, instead pointing to environmental initiators. A hallmark of contemporary culture is a preference for thermally processed foods, replete with pro-oxidant advanced glycation endproducts (AGEs). These molecules are appetite-increasing and, thus, efficient enhancers of overnutrition (which promotes obesity) and oxidant overload (which promotes inflammation). Studies of genetic and nongenetic animal models of diabetes mellitus suggest that suppression of host defenses, under sustained pressure from food-derived AGEs, may potentially shift homeostasis towards a higher basal level of oxidative stress, inflammation and injury of both insulin-producing and insulin-responsive cells. This sequence promotes both types of diabetes mellitus. Reducing basal oxidative stress by AGE restriction in mice, without energy or nutrient change, reinstates host defenses, alleviates inflammation, prevents diabetes mellitus, vascular and renal complications and extends normal lifespan. Studies in healthy humans and in those with diabetes mellitus show that consumption of high amounts of food-related AGEs is a determinant of insulin resistance and inflammation and that AGE restriction improves both. This Review focuses on AGEs as novel initiators of oxidative stress that precedes, rather than results from, diabetes mellitus. Therapeutic gains from AGE restriction constitute a paradigm shift.

Indexed as

AnimalsDiabetes MellitusDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Glycation End Products, AdvancedHumansInsulin ResistanceOxidative StressGlycation End Products, Advanced

Identifiers

PMID21610689
PMCPMC3708644
OpenAlexW2122392577

What OpenQuestion holds

Textmetadata
LicenceTDM
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.