Evidence map›Paper›PMID 22056908›Full record

ReviewFree radical biology & medicine2012

Oxidative stress and diabetes: what can we learn about insulin resistance from antioxidant mutant mouse models?

Jennalynn Styskal, Holly Van Remmen, Arlan Richardson, Adam B Salmon

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 1 pooled it
12.8field-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

114 citing papers in PubMed, 1 synthesis or guideline pooled it, 284 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  7. Review
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  13. NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024
    Review
  14. Review
  15. Article
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  17. Review
  18. Article
  19. Antioxidant and Antidiabetic Activity of Algae.Life (Basel, Switzerland) · 2023
    Review
  20. Review

54 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

4 authors at 3 institutions in 1 country.

Jennalynn StyskalThe Sam and Ann Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78245-3207, USA.
Holly Van Remmen
Arlan Richardson
Adam B Salmon
Geriatric Research Education and Clinical Center · USSouth Texas Veterans Health Care System · USThe University of Texas Health Science Center at San Antonio · US

Funding

TRAINING GRANT ON THE BIOLOGY OF AGINGT32AG021890 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Erzsebet Kokovay, JAMES FLOYD NELSON · 2003 to 2026
$11.4M
ROLE OF CASPASE-2 IN OSTEOCOLAST APOPTOSIS AGE-EePENDENT OSTEOPOROSISP01AG019316 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HERMAN, BRIAN A. · 2001 to 2011
$11.3M
TRANSGENIC ANIMAL CORE SUBCONTRACT WITH UTHSC AT SAN ANTONIOP01AG020591 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI BROOKS, SUSAN V · 2002 to 2014
$10.7M
Role of Oxidative Damage to Specific Molecules in AgingR01AG023843 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI RICHARDSON, ARLAN G. · 2003 to 2007
$1.8M
Protein Oxidation as a Factor in the Mechanism of AgingR37AG026557 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI RICHARDSON, ARLAN G. · 2005 to 2009
$1.2M
TRANSGENIC MICE, AGING, CANCER, AND OXIDATIVE DAMAGER01AG015908 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI RICHARDSON, ARLAN G. · 1998 to 2001
$366k
BLRD VA I01 BX000517NIA NIH HHS P01 AG019316NIA NIH HHS P01 AG020591NIA NIH HHS P01AG020591NIA NIH HHS P01AG19316NIA NIH HHS R01AG015908NIA NIH HHS R01 AG023843NIA NIH HHS R01AG023843NIA NIH HHS R37 AG026557NIA NIH HHS R37AG026557NIA NIH HHS T32 AG021890
6 · The paper itself

Abstract

The development of metabolic dysfunctions like diabetes and insulin resistance in mammals is regulated by a myriad of factors. Oxidative stress seems to play a central role in this process as recent evidence shows a general increase in oxidative damage and a decrease in oxidative defense associated with several metabolic diseases. These changes in oxidative stress can be directly correlated with increased fat accumulation, obesity, and consumption of high-calorie/high-fat diets. Modulation of oxidant protection through either genetic mutation or treatment with antioxidants can significantly alter oxidative stress resistance and accumulation of oxidative damage in laboratory rodents. Antioxidant mutant mice have previously been utilized to examine the role of oxidative stress in other disease models, but have been relatively unexplored as models to study the regulation of glucose metabolism. In this review, we will discuss the evidence for oxidative stress as a primary mechanism linking obesity and metabolic disorders and whether alteration of antioxidant status in laboratory rodents can significantly alter the development of insulin resistance or diabetes.

Indexed as

Insulin ResistanceOxidoreductasesSignal TransductionAnimalsAntioxidantsBlood GlucoseDiabetes Mellitus, Type 2Diet, High-FatDisease Models, AnimalGene DeletionGene ExpressionHumansInsulinMiceMice, KnockoutObesityAntioxidantsBlood GlucoseInsulinOxidoreductases

Identifiers

PMID22056908
PMCPMC3249484
OpenAlexW2026841676

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.