Evidence map›Paper›PMID 21239612›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2011

Role of reactive oxygen species in injury-induced insulin resistance.

Lidong Zhai, Scott W Ballinger, Joseph L Messina

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The role of the Nrf2/Keap1 pathway in obesity and metabolic syndrome.Reviews in endocrine & metabolic disorders · 2015
    Review
  8. Article
  9. Regulation of hepatic insulin receptor activity following injury.American journal of physiology. Gastrointestinal and liver physiology · 2014
    Article
  10. Article
  11. Article
  12. Stress-induced hyperglycemia is a valuable biomarker in febrile neutropenia.Revista brasileira de hematologia e hemoterapia · 2013
    Article
  13. Review
  14. Article
  15. Article
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

3 authors at 2 institutions in 1 country.

Lidong ZhaiDepartment of Pathology, The University of Alabama at Birmingham, 1670 University Boulevard, Birmingham, Alabama 35294-0019, USA.
Scott W Ballinger
Joseph L Messina
University of Alabama at Birmingham · USBirmingham VA Medical Center · US

Funding

Why is the prevalence of obesity so high in U.S. Southern States? Regional predictors of BMI and obesity treatment response.P30DK056336 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI James O Hill · 2000 to 2026
$31.9M
UAB Diabetes Research and Training CenterP60DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GARVEY, W TIMOTHY · 2008 to 2012
$8.4M
Hepatic Insulin Resistance Following HemorrhageR01DK062071 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MESSINA, JOSEPH LOUIS · 2004 to 2013
$2.9M
Gestational cigarette smoke exposure increases adult CVDR01HL077419 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BALLINGER, SCOTT W. · 2004 to 2008
$1.7M
NHLBI NIH HHS HL 77419NHLBI NIH HHS R01 HL077419NIDDK NIH HHS DK 62071NIDDK NIH HHS P30 DK056336NIDDK NIH HHS P60 DK079626NIDDK NIH HHS R01 DK062071
6 · The paper itself

Abstract

Acute insulin resistance is common after injury, infection, and critical illness. To investigate the role of reactive oxygen species (ROS) in critical illness diabetes, we measured hepatic ROS, which rapidly increased in mouse liver. Overexpression of superoxide dismutase 2, which decreased mitochondrial ROS levels, protected mice from the development of acute hepatic insulin resistance. Insulin-induced intracellular signaling was dramatically decreased, and cellular stress signaling was rapidly increased after injury, resulting in the hyperglycemia of critical illness diabetes. Insulin-induced intracellular signaling, activation of stress (c-Jun N-terminal kinase) signaling, and glucose metabolism were all normalized by superoxide dismutase 2 overexpression or by pretreatment with antioxidants. Thus, ROS play an important role in the development of acute hepatic insulin resistance and activation of stress signaling after injury.

Indexed as

AnimalsAntioxidantsBlood GlucoseBlotting, WesternGenotypeGlucose Tolerance TestHemorrhageInsulinInsulin ResistanceLiverMiceMice, Inbred C57BLMice, TransgenicOxidative StressReactive Oxygen SpeciesSignal TransductionAntioxidantsBlood GlucoseInsulinReactive Oxygen SpeciesSuperoxide DismutaseSuperoxide Dismutase 2

Identifiers

PMID21239612
PMCPMC3045736
OpenAlexW2127334967

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.